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M.D., F.R.C.P.E., F.R.S.E. 

Assistant Editors 

M.B., F.R.C.P.E., F.R.S.E., M.R.C.P.Lond. 

M.B., Ch.B. 




; Dt-ocit 


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A Puu for the Study of the Intermbdio-Lateral Cell-System 
of the Spinal Cord. By Alexander Brace, M.A., M.D., and 
J. H. Harvey Pirie, B.Se., M.B. ..... 

A Report of Two Cases of General Paralysis with Focal 
Symptoms. By August Hoch, M.D. .... 

Circumscribed Hemorrhagic Cortical Encephalitis, with the 
Report of a Case in which the Lesion was limited to 
■the Motor Zone, the Chief Clinical Manifestation being 
Jacksonian Epilepsy. By Chas. E. Mills, M.D. 

Eight Cases of Hereditary Spastic Paraplegia. By Ernest Jones, 
M.D., M.R.C.P. (Lond.). 

Am Investigation into the Arrangement of the Achromatic 
Substance of Nerve Cells, and of the Changes which 
it Undergoes in Vajuoub Forms of Mental Diseases. By 
W. Maule Smith, M.D., M.R.C.P.E. .... 

Tabetic Atrophy of the Auditory Nerve. By Sir William R. 

Gowers, M.D., F.R.S. ...... 

• • • • • 

Alcoholic Psychoses : A Study of their Mechanism and of their 
Relation to other Mental Disorders. By C. W. Chapin, 
R.P. ........ 

Dementia Precox. By John Macpherson, M.D. 

Epidemic Cebebro-Spinal Meningitis. By J. S. Fowler, M.D., 

F. R.C.P.E.... . . . . 

A Plea for the Scientific Treatment of Stammering. By 
Hamilton Graham Langwill, M.D., F.R.C.P.E. 

Return of Paraplegia in a Case of Old Infantile Paralysis. 
By Dr O. Crouzon....... 

A Clinical and Experimental Investigation into the Lympho¬ 
genous Origin of Toxic Infection of the Central Nervous 
System. By David Orr, M.D., and R. G. Row, M.D. . 

On the Nature of the “Faisceau bn IEcharpb ” of F4r& By 

G. Elliot Smith, M.D. ...... 

On Another Form of Anomaly in the Cbrbbbo-Pontine Tract. 
By G. Elliot Smith, M.D. ...... 


















The Relative Order of Innervation of Certain Muscles of the 
Arm. By Ashley W. Mackintosh, M.D. .... 

The Occasional Long Duration of Brain Tumour, with the 
Report of a Case of Jacksonian Epilepsy of Eight Years’ 
Duration as the only Sign of a Small Cerebral Glioma. 
By William G. Spiller, M.D., and Edward Martin, M.D. 

The Amyotrophy of Chronic Lead Poisoning: Amyotrophic 
Lateral Sclerosis of Toxic Origin. By S. A. E. Wilson, 
M.A., M.B., B.Sc. ....... 

Further Bacteriological and Experimental Investigations into 
the Pathology of General Paralysis and Tabes Dorsalis. 
By W. Ford Robertson, M.D., and Douglas M‘Rae, M.B., C.M., 

Psycho-Epilepsy. By Sir William R. Gowers, M.D., F.R.S. . 

Remarks on Myoclonus-Epilepsy, with Report of a Case. By 

L. Pierce Clark, M.D. ...... 

A Simplified Technique for Accurate Cell Enumeration in 
Lumbar Puncture. By Ernest Jones, M.D., M.R.C.P. 

The Symptoms due to Peripheral Neuritis or Spinal Lesions in 
Diabetes Mellitus. By R. T. Williamson, M.D., F.R.C.P. . 

The Pathology of Epidemic Cerebro-Spinal Meningitis. By 

Stuart M‘Donald, M.D., F.R.C.P.E. ... 593, 

A Case of Narcolepsy. By Sir William R. Gowers, M.D., F.R.S. . 

Landry’s Paralysis. By A. Lewin Sheppard, M.B., B.S., and 
I. Walker Hall, M.D. 

Observations on the Treatment of General Paralysis and 
Tabes Dorsalis by Vaccines and Anti-Sera. By W. Ford 
Robertson, M.D., and Douglas M‘Rae, M.B., C.M., M.R.C.P.E. . 

The Exact Determination of Areas of Altered Sensibility. By 
Wilfred Trotter, M.S., F.R.C.S., and H. Morriston Davies, M.C. 
(Cantab.), F.R.C.S. ...... 

Case of Trigeminal Njevus, associated with Epilepsy and Contra- 
Lateral Hemiparesis. By J. W. Struthers, F.R.C.S.Ed. 

The Mechanism of the Plantar Reflex, with Especial Refer¬ 
ence to the Phenomenon of Crossed Reflex. By Philip 
Coombs Knapp, A.M., M.D. ..... 

Arterio-Sclerosis in Relation to Mental Disease. By C. Macfie 
Campbell, B.Sc., M.B., Ch.B. ..... 

Unusual Sequela of Herpes Zoster (? Posterior Poliomyelitis). 

By Alexander Bruce, M.D., Etc. ..... 





















fie urology ant> ps^cbtatr^ 

Original articles 



Physician to the Edinburgh Royal Infirmary ; 



C linical Tutor in the Medical Wards, Edinburgh Royal Infirmary. 

Our main object in bringing this communication before the 
Society is to draw attention to the importance of the study 
of a system of nerve cells in the spinal cord which, in our 
opinion, appears to deserve more attention than it has yet 
generally received. We are all more or less familiar with the 
large motor cells in the anterior horns of the cord: their 
distribution is well known, as are also many of the pathological 
changes which they undergo, and considerable progress has been 
made in the establishment of their relation to the innervation of 
individual muscles. In like manner with regard to the cells of 
the vesicular column of Clarke, much is already known. Its 
distinctness as a group, and the characteristic form of its cells, 
so unlike anything else in the cord, has led to recognition of its 
exact position and distribution in the cord, and recent methods 
of research appear to have proved beyond doubt that its axones 

1 A paper read before the Medico-Chirurgical Society of Edinburgh on November 7, 

B. OF N. & P. VOL. V. NO. 1—A 


are continued into the direct cerebellar tract of Flechsig. In 
addition, however, to these two outstanding cell-systems, there 
remain at least two other which have not received the same 
amount of study. There are large numbers of small polygonal 
cells scattered irregularly at the base of the anterior horns, whose 
function and distribution still remain to be determined; and, 
secondly, there is the cell-system which forms the subject of our 
communication to-night. 

This cell-system was first observed by Lockhart Clarke in 
1851. In 1859, in a second paper read before the Royal 
Society of London, he described more fully the distribution 
and character of the cells, and gave it the name “ intermedio- 
lateral tract,” which it now generally bears. This term, as used 
by Clarke, indicates that it is a tract, column, or system of nerve 
cells situated along the lateral margin of that portion of the grey 
matter which is intermediate between the anterior and posterior 
cornua. Clarke stated also that the tract extended from the 
lower end of the cervical to the upper end of the lumbar 
enlargement, and that it was not found in these enlargements, 
but reappeared above and below them. 

For a long time after the publication of Clarke’s papers, 
anatomists seem to have in the main contented themselves with 
merely noting its existence, and tended to locate it in the apex 
of the lateral horn of the cord. It was only gradually that it 
became recognised that the lateral horn in which the tract was 
located was not the same as the lateral projection of the anterior 
horns in the lumbar and cervical enlargements, and that the cells 
of the intermedio-lateral tract were of different form and character 
from those of the anterior cornua. It was not until Waldeyer 
published in 1888 his classical paper on the spinal cord of the 
gorilla that any material advance in our knowledge was made. 
Waldeyer showed that the tract was situated not merely in the 
lateral horn of the grey matter, but that it extended backwards 
as far as the angle between the lateral and posterior horns, to 
a point in immediate relation to the formatio reticularis. While 
agreeing with Clarke that the cells of that part of the tract 
which was situated in the lateral horns are not found in the 
cervical and lumbar enlargements, he traced those cells overlying 
the formatio reticularis through both enlargements, thus making 
the intermedio-lateral cell-system co-extensive with the spinal cord. 



In 1905 one of ns (A. B.) submitted the intermedio-lateral 
tract to an exhaustive examination by means of serial sections, 
and arrived at the following, amongst other conclusions :— 

(a) In agreement with Waldeyer, that the intermedio-lateral 
tract was composed of cells in and near the tip of the lateral 
horn (which may be termed apical cells), and also of cells at the 
angle of the formatio reticularis (the reticular cells). 

(5) That the upper limit of the tract was in the middle of 
the eighth cervical segment, and the lower limit at the lower 
end of the second, or possibly at the upper end of the third 
lumbar segment. 

(c) That the cells were arranged in peculiar groups or masses, 
sometimes quite separated from each other and sometimes quite 

(d) That these groups were apparently characteristic for each 
segment, and were on the whole fairly symmetrical on the two 

(e) That the number of the cells was immensely greater than 
has been hitherto realised. 

The following are the total numbers counted in each 



C. 8 



D. 1 



D. 2 



D. 3 



D. 4 



D. 5 



D. 6 



D. 7 



D. 8 



D. 9 



D. 10 



D. 11 



D. 12 



L. 1 



L. 2 



Total 88,577 




Other points were established, but for these the original 
paper in the Transactions of the Boyal Society of Edinburgh, 
VoL xlv., Part 1, 1906, may be consulted. 

It cannot be said that the possible function of the inter- 
medio-lateral cell-system was seriously considered until Gaskell 
published his epoch-making paper on the sympathetic system 
in the Journal of Physiology in 1886. In this paper he showed 
that while all the roots of the spinal cord were connected with 
ganglia of the sympathetic system by means of fine non- 
medullated fibres (grey rami communicantes), only a limited 
number of these roots were also connected with sympathetic 
ganglia by fine medullated fibres (white rami communicantes). 
That limited number extended from the second (afterwards 
corrected to the first) thoracic or dorsal to the third or fourth 
lumbar in the cat. Besides these there were two additional 
white rami from the lower sacral cord. Gaskell was struck 
by the fact that the longitudinal extent of origin of these white 
rami corresponded with that of the vesicular column of Clarke 
and suggested that this column was probably the spinal centre 
for these fibres. Subsequently he stated that the intermedio- 
lateral tract also acted as a centre of origin. It will be noted 
that the longitudinal distribution of the cells of the intermedio- 
lateral tract corresponds exactly with that of the origin of the 
white rami. The mere existence of such a coincidence is not in 
itself sufficient, however, to establish a connection between the 
cells of the intermedio-lateral tract and the white rami com¬ 
municantes. The most satisfactory way to prove this would no 
doubt be to trace the fine fibres directly from the cells to the 
anterior roots from which the white rami arise. That still 
remains to be done. The problem has, however, been attacked 
in another way, namely, by studying the changes which take 
place in the cells of the cord after division of nerve roots 
emerging from it. It is now established that under certain 
circumstances, by some retrograde influence, the cells connected 
with the divided nerve fibres undergo a peculiar and easily 
detectable change, viz. a displacement of the nucleus towards 
one surface, and a disappearance of the chromatic granules. 
To this process the term reaction & distance has been applied. 
It may be regarded as demonstrated that if, after the section 
of a bundle of nerve fibres, certain nerve cells degenerate in the 



way mentioned, these cells are connected with the divided fibres. 
By these means it has been found by Anderson that, on dividing 
the cervical sympathetic, the cells of the intermedio-lateral tract 
in the upper region underwent the reaction & distance. His 
results have been completely confirmed by Herring, who found 
a degeneration of the cells in the tract beginning above at the 
level of the superficial origin of the eighth cervical root, being 
most marked at the level of the first and second dorsal, and 
diminishing downwards as far as the sixth dorsal segment. Both 
these observers found that the cell-change did not extend beyond 
the intermedio-lateral tract 

Onuf and Collins, however, have given a more extensive 
origin to the sympathetic fibres, tracing it not only into the 
lateral columns, but into certain paracentral cells, into cells in 
the posterior cornua, etc., while Biedl has actually found after 
section of the splanchnics a degeneration in the lateral horns of 
the lowest cervical, and in the anterior horns of the upper dorsal 
extending as high as the sixth cervical and as low as the fifth 
dorsal nerve. Other observers have found an even more ex¬ 
tensive degeneration, but their results are of such a nature as to 
suggest some flaw in the operative or histological technique. It 
appears to us on reviewing the literature, that it is justifiable to 
assume that the origin of the cervical cord is as Anderson and 
Herring have stated it, and that the analogy of the relationship 
of the splanchnics to the cord suggests a similar origin. Of 
this, however, an absolutely complete experimental proof still 
remains to be made. 

Gaskell arrived at the conclusion that the white rami were 
efferent fibres, and that of those some terminated in vertebral 
ganglia, others passed through these and terminated in pre- 
vertebral ganglia, which lay in more or less immediate relation 
to viscera. He made the bold generalisation that those which 
terminated in the vertebral ganglia were vaso-motor, while those 
which terminated in the distal or prevertebral ganglia were all 
va 80 - or viscero-inhibitory. This view has not been upheld, 
and we owe to Langley, Anderson, Schafer, Rose Bradford, 
Bayliss and Starling, Francis Franck, and other workers too 
numerous to mention here, the establishment by the sounder 
method of experiment of the functions of the various roots. If, 
as seems justifiable, we may infer that the effects produced 



by stimulation of the roots represent some, if not all, of the 
effects resulting from the normal action of the cells of origin of 
these roots, then we obtain by these experimental methods data 
as to the functions of the different parts of the intermedio- 
lateral tract. 

The accompanying table shows the effects of stimulating the 
various roots of the sympathetic systems. 

Dilatation of Pupil (1) . .12 3 

Retraction of Nictating Mem¬ 
brane: Separation of Eyelids; 

Protrusion of Eye (1) . .12 3 4 

Blood-Vessels of Head (1) . (1)2 3 4 

Secretion of Submaxillary 
Gland in Cat (1) . . . (1) 2 3 4 

Acceleration of Heart (1) .12 3 4 

Hairs of Face and Neck (1) (3) 4 

Vaso-Motor Fibres to, and 
Sweat Glands of, Fore- 
Foot (1) 4 

Spleen (2) . (3) (4) 

Vaso-Constrictora of Portal 
System (8) . . . . (3) 4 

Viscero-Motor and Viscero- 
Inhibitory to Small Intes¬ 
tine (4) 

Inhibitory to Small Intes¬ 
tine (5) 

Vaso-Motor to Liver, Pancreas, 

Small Intestine; 1st Part of 
Large Intestine (6) 

Vaso-Motor to Kidney (7) 4 

Vaso-Motor and Sweat Secre¬ 
tion of Hind-Foot (1) . 




5 ( 6 ) 

8 6 7 

5 6 7 8 9 (10) 

5 3 7 8 9 10 (11) (12) (13) (1) 

5 0 7 8 0 10 (11) 

6 7 8 0 10 11 12 13 1 2 (3) ( 4 ) 

6 7 8 9 10 11 12 13 1 

(5) 6 7 8 9 10 11 12 13 1 2 

5 6 7 8 9 10 11 12 13 (1) (2) ( 3 ) ( 4 ) 

11 12 18 1 2 3 

The numbers within brackets Indicate levels where the resulting stimulation was faint, Inconstant, or 

Tbe numbers In heavy type indicate lerela at which stimulation gave the maximum result. 

1 Langley, 44 Schafer’s Physiology,” Vol, ii., p. 616, et seq., with further re¬ 
ferences to literature. 

a Schafer and Moore. Virchows Arch., 1877, p. 181. 

1 Baylissand Starling. Joum. Physiol ., Vol. xrii., p. 120. 

4 Bunch. Joum . Physiol ., Vol. xxiL, p. 867. 

5 Bechterew and Mislawsky. Arch . de Physiol . norm, et path., 1889, p. 248. 

• Francis Franck and Hallion, Ibid., 1896 and 1897. 

7 Bradford. Joum. Physiol., 1896, p. 858. 



All the sympathetic fibres for the upper part of the body, 
with the exception of those for the acceleration of the heart 
and for the sweat secretion and circulation of the fore-foot, pass 
to the superior cervical ganglion. In the two exceptions men¬ 
tioned the fibres terminate in the ganglion stellatum. Those 
fibres which innervate the abdominal viscera pass into the solar 
ganglia. The fibres for the circulation and sweat secretion of 
the hind foot enter the sixth and seventh lumbar and the first 
and second sacral ganglia. 

These anatomical and physiological details would only have 
an academic value for us, and would not be in place at a meeting 
of our Society unless they could be linked up to clinical and 
pathological facts. We are in a position to bring before the 
Society notes of two cases in which the symptoms indicated an 
involvement of the sympathetic system, and in which we have 
found lesions of the intermedio-lateral tract at levels suggested 
by the results of physiological experiment—lesions which there¬ 
fore appear to us to be adequate to have produced the symptoms 
in question. 

In one case loss of sweating in the lower extremities had 
developed during the course of an acute atrophic paralysis in an 
adult. The other case was one of acute exophthalmic goitre, in 
which death took place during an access of hyper-thyroidism. 

Cask I. X. Y., unmarried, aged 30, had been in somewhat imperfect 
general health for a considerable number of months, owing to a succession of 
attacks of influenza and to overwork. For some three months previous to the 
acute onset of his illness he had complained of pains about the middle of the 
dorsal region, and in the shoulders and feet. There had also been several 
crops of purpuric spots on the feet and legs. These, as well as the pains 
referred to, had been regarded as probably of rheumatic origin. On one 
occasion some difficulty of micturition had been noted, and some ten days or 
■o previous to the sudden onset of the paralysis this difficulty recurred. 
There also appeared a slight tendency to stumble while walking, some un¬ 
steadiness in standing, and a degree of tingling and numbness in both lower 
extremities, particularly in the right. These symptoms were attributed 
simply to weakness, and, although the patient always felt very tired, he con¬ 
tinued to take a certain amount of exercise. On the 1st of September he 
noted that he walked with difficulty, and felt much exhausted after a short 
game of golf. On the night of the 1st September 1905 he slept soundly, and 
on waking found that he was completely paralysed, both as to motion and 
sensation, from the waist downwards. 



On examination, on the 4th September, there was complete flaccid 
paralysis of the muscles of the abdomen and of both lower extremities. 

There was almost complete loss of all forms of sensibility below the level 
of the 5th intercostal space, although there were still some slight traces of 
tactile sensibility in the skin of the abdomen. At the 5th intercostal space 
sensibility was impaired, and there was no hypersesthetic zone. Above the 
5th interspace, sensation and motor power were quite intact. There was no 
pain or tenderness over any part of the spinal column or elsewhere in trunk 
or limbs. 

The deep reflexes of the lower limbs were entirely absent. On tickling 
the soles of the feet, there was no response on the left, and a doubtful 
extensor response on the right side. The cremasteric and abdominal reflexes 
were present on both sides. 

Slight twitching movements of the right leg occurred frequently. There 
was retention of urine and faeces. The temperature was 101-102° F. The 
heart, lungs, and urinary system were normal. Apart from the above- 
mentioned influenzal and rheumatic attacks, patient had suffered from no 
other diseases of importance, except the ordinary infectious diseases of child¬ 
hood. The family history was unexceptionable. 

Progress of the cate as regards :— 

1. Motility. 

From the date of the first examination till the date of death, on January 
10th, 1906, there was never the slightest return of any voluntary motor 
power in the lower limbs. The muscles remained flaccid throughout and 
atrophied very rapidly. 

The knee-jerks remained constantly absent, and the plantar reflexes were 
seldom obtainable, although it was thought that there was occasionally an 
indefinite extensor response on the right side. The anal reflex was marked, 
and the sphincter ani retained its tone. 

The patient suffered much from muscular twitchings and jerkings in both 
lower extremities, anterior abdominal wall, and muscles of the lower part 
of the back. These twitchings were sometimes slight, almost tremor-like ; at 
other times large, strong jerks, moving the limbs and bending the back. They 
were considerably influenced by posture, occurring most frequently when the 
patient was lying on his back, but almost invariably ceasing when he was 
turned on one or the other side. 

Passage of a catheter not infrequently set up strong, almost tetanic con¬ 
traction of the recti abdominis ; frequently also the constrictor urethrae went 
into spasm, which effectually prevented the passage of the instrument 

2. Sensibility. 

Touch .—Sensibility to light touch began to return within a few days of the 
onset and returned over the lower part of the trunk, the whole of the left 
lower limb and most of the right, except the outer side of the leg and part of 
the inner side about the ankle. There was a spot on the ball of the right 
great toe where the tactile sensibility was particularly acute. Elsewhere the 
return of sensibility was not equally perfect, however, and touch was not 



always correctly localised. The patient never felt the passage of the catheter, 
but there was a slight degree of sensibility in the rectum. 

Pain Sense .—In the course of a fortnight there was a slight return of 
sensibility to pain over the lower dorsal areas, particularly on the left side, 
and in the same region there was a slight appreciation of heat and cold. 
Below this level there was no return of sensibility to pain or temperature. 

Throughout the greater part of the course of the illness there was a marked 
subjective sensation of cold in the paralysed areas. This might appear 
spontaneously after perspiration, or after the slight exposure necessary for 
nursing purposes. It was present even with a considerable degree of fever, 
when the skin felt hot and dry to the touch. It often resembled what is 
found during the cold stage of a malarial attack. 

3. Tbophic Functions. 

In addition to the muscular wasting of the lower extremities already noted, 
there was a marked and rapid wasting of the whole body. 

Within a few days of the onset of the disease, several small bulla? formed 
on the left tibia and on the inner Bide of the right knee, and a small sub¬ 
cutaneous haemorrhage where the knee had been allowed to come into contact 
with the other leg. 

On the dorsum of the right foot several erythematous patches appeared, 
and over the outer malleolus a small bulla like those on the left leg. With 
care and suitable treatment these all healed. 

A fortnight after the onset there appeared over the tip of the sacrum a 
small sore—not a typical bed-sore, but rather a haemorrhagic spot, although 
the skin over it gave way. This healed, but about six weeks from the com¬ 
mencement of the disease, typical bed-sores appeared on the buttocks, and, 
despite all treatment, gradually increased in size and were with difficulty kept 
from becoming septic sores. 

4. (a) Micturition. 

At first there was complete retention, but after three weeks the function 
became of the involuntary automatic type, i.e. the urine accumulated in the 
bladder until a certain pressure was reached, then a contraction set in, the 
tension of the “ internal sphincter ” was overcome, and a certain amount of 
mine was forcibly ejected. The bladder was never completely emptied, 
however, a certain amount of residual urine always remaining. 

Cystitis very rapidly ensued, and the bladder had to be regularly 
washed out. The capacity of the bladder gradually diminished; 12 to 15 oz. 
of residual urine were usually present at first; this gradually diminished 
until at the end only about 1 oz. remained. The introduction of a corre¬ 
sponding amount of boracic lotion always caused a forcible contraction. 
There was no sensation connected with micturition. The sense of pressure 
usually associated with a full bladder was also absent. 

( b ) Deprecation. 

At first there was complete inaction of the lower bowel; later the action 
of the bowels could be kept fairly regular with the aid of medicine and of 



occasional enemata. Although the movement of the bowels was entirely 
beyond the control of the will, certain indefinite sensations usually made the 
patient aware of the approaching passage of faeces, although these were also 
passed sometimes unconsciously. 

5. Temperature and Sweating. 

Patient’s temperature was of a hectic, swinging type during all four 
months, at first ranging from 99-101°. After a fortnight it fell almost to 
normal for a few days, but again began to rise and fall, and gradually the 
minima rose till the temperature was seldom below 101-102°. On one occasion 
the temperature rose as high as 106’. The time of occurrence of these eleva¬ 
tions of temperature was quite irregular. With many of them there were 
rigors or shiverings followed by profuse perspirations. The distribution of 
the sweating was remarkable. Above the level of the sixth intercostal nerve 
after each attack of fever, the perspiration was very profuse. Below a sinuous 
line situated about two and a half inches above Poupart’s ligament there was 
absolute loss of sweating, except over a small area on the 
inner side of both thighs. Between this sinuous line 
and the level of the fifth dorsal nerve the skin of the 
abdomen perspired in irregular patches. The area from 
which perspiration was entirely absent is shown in Fig. 1. 

7. General Condition. 

The patient’s condition became gradually worse, in 
spite of all treatment. The heart and lungs were unin¬ 
volved. A fair quantity of nourishment was taken, but 
despite this there was emaciation progressing to an 
extreme degree. The mental capacities ultimately be¬ 
came gradually dulled, and death ensued from sheer 
exhaustion, four months after the onset. 

Permission was obtained for an examination of the 
spinal cord. 

Examination of the Cord. 

Examination of the spinal cord showed that 
the meninges were throughout its whole length 
quite normal. The cord was smaller than 

Pig. 1 .—The area from which “onnal, and the lumbosacral enlargement was 
sweating was absent is in- somewhat soft in consistence. The anterior 

dicated in black. Note spinal vein was dilated. The veins of some 
the small unshaded area * . 

on the inner side of both of the posterior roots m the lower dorsal and 

thighs. lumbo-sacral region were greatly dilated. 

On section of the cord, the grey matter in the lumbar and 

sacral enlargements was so greatly congested as to have an 



almost general red colour, on which minute haemorrhages could 
be distinctly seen. This congestive and haemorrhagic condition 
extended into the lower dorsal region and gradually diminished 
in an upward direction, ceasing altogether about the level of the 
sixth or seventh dorsal segment. 

Microscopical Examination. 

At the levels of the lower dorsal segments and the lumbo¬ 
sacral enlargements, partially organised thrombi were found in 
the anterior spinal vein (which they did not, however, com¬ 
pletely occlude), and also in some of the arteries of the posterior 
roots and in a few of the lateral coronary branches passing 
towards the intermedio-lateral tract. 

The grey matter of the anterior cornua displayed a great 
congestion of its arterioles and capillaries. A similar congestion 
could be seen in the base of the posterior cornua, in the lateral 
cornua, and in the margin of the grey matter between the lateral 
and posterior horns. In the anterior horn the finest capillaries 
were all greatly injected and tortuous, and there were very 
numerous minute haemorrhages. In a considerable number of 
instances the extravasated blood had found its way into the 
lymphatic spaces surrounding the motor nerve cells of the 
anterior cornua. Red cells were also frequently seen in the 
perivascular spaces, and also more or less scattered throughout 
the neuroglia. A careful search throughout the whole of the 
affected area failed to show any escape of leucocytes or any 
definite proliferation of the connective tissue cells. The motor 
cells in the affected area were almost all in a state of degenera¬ 
tion, the degree of which, however, varied within wide limits. 
A few apparently healthy cells, with well-marked polygonal out¬ 
line and a centrally-placed nucleus and deeply staining, sharply 
defined tigroid bodies, were seen scattered irregularly amongst 
other markedly degenerated cells. The majority of the cells, 
however, showed displacement of nucleus. In a large number 
the nucleus was either close to or projected out from the 
periphery of the cell. There was a marked chromatolysis, 
the tigroid bodies being replaced by a turbid, finely granular 
cytoplasm. Within this cytoplasm there were not infrequently 
vacuoles varying in size. In a great many of the cells there 
were also masses of golden-yellow granular pigment, in some large 



enough to occupy almost the whole cell. The affected cells were 
swollen, and had largely lost their angular, polygonal outline, 
their dendrites being markedly retracted. As already stated, 
there was a marked congestion of the vessels in the lateral 
cornua, and nearer examination revealed the fact that there were 
numerous small haemorrhages amongst the cells of the intermedio- 
lateral tract, both at the apex of the lateral horn and in the 
reticular group of cells. There were also on both sides almost 
symmetrical haemorrhages in the vessels leading from the surface 
of the cord to the tip of the lateral horn, and also from others 
within the substance of the formatio reticularis close to the 
margin of the grey matter. A few vessels in the substance of 
the formatio reticularis were found to be completely thrombosed, 
and one or two minute arterioles contained organised thrombi. 
Throughout the tenth, eleventh, .and twelfth dorsal and the first 
and second lumbar segments, both the apical and reticular groups 
on both sides of the intermedio-lateral tract showed degenerative 
changes analogous to those found in the large motor cells of the 
anterior cornua, the cells showing marked lateral displacement 
of nuclei (see Figs. 2 and 3), and disappearance more or less 
complete of chromatic granules. Some of the cells were also 
remarkably swollen and their shape distorted. 

Similar degenerative changes were found in the small 
polygonal cells of the anterior cornua (Waldeyer’s “ middle 
cells ”), and also in the large solitary cells of Schwalbe in the 
posterior cornua. The cells of Clarke’s column appeared unduly 
swollen, and many showed complete chromatolysis. The known 
variety of changes in normal cells of this system make it diffi¬ 
cult to speak definitely as to the incidence of degeneration. In 
the lateral columns of the lower dorsal, lumbar and sacral enlarge¬ 
ments there was a degree of sclerosis in the pyramidal tract. 
The direct cerebellar tract was only very slightly affected, a fact 
which would indicate that the cells of the column of Clarke had 
escaped degeneration. 

In considering this case we have to draw special attention to 
two outstanding features : the extensive degree of acute atrophic 
paralysis and its association with vascular paresis in the lower 
limb, and the loss of sweating in almost the whole of the lower 
part of the body below a level drawn about two inches above 
Poupart’s ligament. The first explanation that might naturally 



suggest itself is that one lesion is responsible (or the motor 
paralysis and for the loss of the fnnction of perspiration; but the 
association of the two conditions is too rare for that possibility to 
be entertained. It is remarkable how seldom a persistent dry¬ 
ness of skin is referred to in cases of acute atrophic paralysis due 
to lesions of the anterior cornual cells, and it is obvious that the 
muscular paralysis and atrophy must be attributed to the affec¬ 
tion of the anterior cornua, and that the residual symptoms of 
the vaso-motor and secretory disturbances in the skin must be 
attributable to some additional lesion. That additional lesion is 
in all probability the haemorrhage and congestion, and the con¬ 
sequent degeneration of the cells of the intermedio-lateral tract 
in the tenth, eleventh, and twelfth dorsal and in the first and second 
lumbar segments. This corresponds fairly closely to the levels 
where Langley has found that stimulation of the sympathetic 
roots causes sweating in the hind foot of the dog. It is evident 
from Higier’s and Schlesinger’s writings that there is a special 
area for sweat secretion in the lower limb, corresponding closely 
to that found in our case, and we would suggest that in similar, 
or in more limited affections of vaso-motor and secretory dis¬ 
turbances in the lower limb, a special examination of this area of 
the intermedio-lateral tract should be made. 

The second case in which we have found a lesion of the 
intermedio-lateral tract was one of exophthalmic goitre, in 
which death took place apparently from hyperthyroidism. The 
opportunity of examining the spinal cord of this case we owe to 
the kindness of DrGulland, who has supplied the following notes:— 

Case II. Mrs M., aged 47. Admitted to Chalmers’ Hospital on 22nd May- 
1906. Died 5th June. Duration of illness, eleven months. Began with an attack 
of diarrhoea eleven months ago, since when she has been nervous and weak. 
Swelling of the neck was noticed first in January 1906. Exophthalmos was 
not noticed by her friends. 

Status Prvesens .—Marked tremor ; slight exophthalmos. Bight lobe of 
thyroid most enlarged. Pulse averages 120 to 130. Presystolic and systolic 
murmurs. No albumen or sugar. Very nervous and excited. 

Course. —Temperature above normal throughout; for the first week ran 
between 98 and 100 ; second week, between 99*5 and 100*5, rose to 103*4 just 
before death. Nothing found in lungs or elsewhere to account for this. 

From June 1st she became very noisy and excited ; pulse became weaker 
and more rapid ; the heart became dilated. Speech became inarticulate ; 
excreta were passed in bed ; urine contained acetone—no sugar. On the 4th 
she became unconscious, and died at 6.10 on the 15th. 



Post-mortem. —Same day. Thymus large ; thyroid large, pale ; very little 
colloid ; active proliferation of gland tissue, so that it presented the appear¬ 
ance of a secreting gland ; some fibrosis. Left supra-renal large and cystic. 
Kidneys showed some chronic interstitial nephritis with an acute toxic con¬ 
dition superadded. Liver : chronic venous congestion, with some fatty change 
and areas of early cirrhosis. Spleen: recent infarcts, acute congestion. 
Stomach: congestion and haemorrhagic infiltration. Heart: right auricle 
dilated, other cavities small, chronic thickening of mitral and aortic valves ; 
no recent endocarditis; some fibrous change in myocardium. Lung: no 
pneumonia; certain amount of oedema and congestion. Marrow was a 
lymphocytic, not a myelocytic marrow. No other abnormalities in the body. 

The spinal cord was handed to us by Dr Wade immediately 
after the post-mortem examination, and placed at once in 10 per 
cent, formalin solution. On the following day, on dividing the 
cord into segments, we observed minute haemorrhages at the outer 
side of the grey matter on both sides at the lower part of the 
2nd, in the 3rd, and in the 4th dorsal segments, and in no others. 
Microscopic examination demonstrated certain lesions in the grey 
matter and in the immediately adjacent white matter. These 
changes were partly in the blood-vessels and partly in the cells 
of the intermedio-lateral tract. The most obvious morbid appear¬ 
ances were capillary haemorrhages. These were almost symmetrical 
as regards position, but were considerably larger on the left side 
than on the right. They were situated at the apex of the posterior 
horns, immediately within the outer margin of the grey matter, 
and extended backwards into the posterior horns and forwards as 
far as the lateral horn. They were apparently quite recent, pro¬ 
bably merely terminal haemorrhages. Another prominent vascular 
change was the hyaline degeneration of the tunica media of the 
arterioles of the lateral columns, which led towards the lateral 
horns, and also of others in the posterior columns directed towards 
the root of the posterior horns. The anterior spinal artery and 
its branches, as well as the coronary branches to the anterior 
cornua, were quite free from this hyaline change. It was pro¬ 
nounced in the lower part of the 2nd, in the 3rd, 4th, and 5th 
segments, but it was also found in a gradually decreasing extent 
in the same group of arterioles as far down as the lower dorsal 

The changes in the nerve cells to which we desire to draw 
special attention, were almost entirely limited to those contained 
in the intermedio-lateral tract. In the 1st dorsal segment there 
was a slight chromatolysis in a few of the cells of the anterior 



cornua, but with this exception the motor cells remained entirely 
normal. In marked contrast to these normal motor cells were 
the cells of the intermedio-lateral tract These in the 3rd and 
4th dorsal segments were, almost without exception, more or less 
affected ; in the 2nd and 5 th the involvement was to a less extent, 
and it was very slight in the 1st and 6th segments. As may he 
seen in Figs. 4 and 5, the abnormal cells showed somewhat similar 
degenerations to those described in our previous case. In a large 
proportion there was a lateral displacement of nucleus, and greater 
or less disappearance of chromatic granules. In addition, some 
of the cells were swollen or vacuolated, while many were shrunken 
and distorted and altogether devoid of nucleus or chromatin. A 
careful examination of the grey matter showed that the cells 
of the intermedio-lateral tract had been practically exclusively 
affected in this special manner. 

It is beyond the purpose of this paper to enter into a dis¬ 
cussion of the question as to whether the nervous lesion or the 
affection of the thyroid is the primary one in exophthalmic 
goitre. We wish in the meantime to content ourselves with 
drawing the attention of the Society to the fact that the segments 
involved are those which experiment shows to be the segments 
which give origin to the roots, stimulation of which produces 
retraction of the upper eye-lid, protrusion of the eye-ball, 
acceleration of the heart, and sweating and vaso-regulation of 
the upper part of the body. We would suggest that future 
investigations of the sympathetic system should include the cells 
of the intermedio-lateral tract of the whole thoracic region, as 
well as the cells of the bulbar autonomic system, which Dana 
has shown to be involved in one case of exophthalmic goitre. 

Onuf and Collins, in their valuable work on the sympathetic 
nervous system, have also drawn attention to the possible con¬ 
nection of the sympathetic cells in the cord with the diseases 
which are known to be of sympathetic origin, and with others 
which are so frequently regarded as being merely due to func¬ 
tional disturbances. Lannois and Porot, in the Revue de Midecine, 
1903, have published a case of erythromelalgia, with gangrene of 
the extremities, associated with extensive involvement of the 
intermedio-lateral tract. With that exception comparatively 
little has apparently been done to establish a relation of lesions 
of the tract with morbid phenomena. A possible explanation 



of this may lie in the fact that changes in the nerve cells may 
be in many instances not obviously destructive, but of a nature 
which can only be demonstrated by modem methods of histo¬ 
logical investigation. It is easy to understand how fine changes 
in cells of a system whose function was not even suspected had 
escaped detection. If we succeed in drawing the attention of 
the Society to the importance of the intermedio-lateral tract, the 
purpose of our paper will have been fulfilled. 

Description or Figures. 

Figs. 2 and 3 represent the appearances presented by the degenerated cells of 
both intermedio-lateral tracts in the lower dorsal and upper lumbar 
region in the case of acute atrophic paralysis. 

Fig. 2.—In the centre of the field is a swollen cell with a partial chromatolysis 
and a displaced nucleus. 

Fig. 3 shows, above and to the left, two cells with partial chromatolysis. In 
the cell to the left the nucleus is displaced upwards and to the left. 
In that to the right the nucleus is situated to the right of the cell. Two 
smaller cells above the two just described show similar displacement of 
nucleus. On the right side of the section and near the centre there are 
other two cells in both of which displacement of nucleus is detectable. 
About one centimetre above the large capillary in the lower part of the 
field is seen a large cell in which the half to the left was pale from the 
presence of a yellow granular pigment. In the right half there was 
marked chromatolysis. 

Figs. 4 and 5 represent the degeneration of cells found in the intermedio- 
lateral tracts, especially in the second, third, fourth, and fifth dorsal 
segments, in the case of exophthalmic goitre. 

Fig. 4.—Middle of second dorsal segment, right half. To the right of the 
centre is a swollen cell showing a granular cell-substance. To the left 
of this is another cell with displacement of nucleus, loss of chromatin 
and a distinct vacuole. In the lower part of the field are other cells with 
displaced nuclei. 

Fig. 5.—Lower end of second dorsal segment, left side. Almost in the middle 
of the field is a swollen cell with loss of nucleus and chromatin 
granules. To the left, above, and to the right of this cell are three cells 
showing distinct displacement of nucleus. That situated above the large 
granular cell also shows small vacuoles. One cell near the top of the 
right half of the field shows also a displacement of nucleus. 


Gaskell. “ Structure and Function of Visceral Nerves,” Joum. Physiol., 1886 
and 1889. 

H. K. Anderson. “Central Origin of the Cervical Sympathetic Nerve,” 
Joum. Physiol., 1902, p. 610. 

Percy T. Herring. “Spinal Origin of the Cervical Sympathetic Nerve,” 
Joum. Physiol., 1903, p. 282. 



Oniif and Collins. “Sympathetic Nervous System,” 1900. 

BiedL “The Splanchnic Centres,” Wien. klin. Wchnschr ., 1895, p. 915. 
Higier. D. Ztschr. f. Nervenheilk., Bd. 30, p. 426. 

Schlesinger. “ Die Syringomyelie,” Leipzig, 1895. 

Lannois and Porot. “ Erythromelalgia, followed by Qangrene of the Ex¬ 
tremities,” Rev. de M&L, 1903, p. 824. 

Further references to bibliography will be found in Schafer’s “ Text-Book 
of Physiology,” VoL ii., and in Bruce’s “Distribution of the Cells in the 
Intermedio-lateral Tract of the Spinal Cord,” Trans, of the Royal Soc. of 
Edinburgh , Yol. xlv., Part 1, 1906. 



Bloomingdale Hospital, White Plains, New York; Instructor in Psychiatry, 
Cornell Medical School, New York. 

Cass I. A well-educated business man, 50 years old. One 
brother is an epileptic. No other heredity is known. No 
serious previous diseases. He had, however, a fall from the 
rigging of a boat three years before the onset of the present 
illness. He was unconscious for a short time, but had no other 
known after-effects. A history of syphilis could not be obtained, 
but the only informant is the sister, and the patient has been 
away from home a good deal 

The history of the patient’s illness could be gathered almost 
only from letters which he wrote to his sister. The following 
are extracts which give not only a fair idea of the development 
of the disease, but also of the difficulty which, even early in the 
disease, the patient experienced in expressing himself in writing. 

February 15th, 1901.—“. . . I go for my health (sc. to Cal.) 
and go as because I have to at once. My head has troubled me 
g continuous way until I could not continue my business. ... I 
can’t write much buct I can’t” 

He consequently went to California on February 18th, and 
there is said to have been somewhat irritable, but nothing else 
is known about him. 

On March 31st, 1901, he writes that this is the first letter he 
has been able to write since he went to California. He gives 





stricken “ with an attack of meningeal apoplexy and was for three 
days paralysed almost completely, including limbs, sphincters, 
sight, and throat.” Two weeks later he writes : “ The patient is 
able to walk, eats solid food, has almost complete control of 
sphincters, but talks and sees imperfectly. He can make his 
wants known ; has been violent at times, but is now very pliable 
and easy to care for.” (A history from the sanatorium could not 
be obtained, though asked for.) 

Early in February 1902 he was brought to Boston, and 
arrived on the 6th. He was taken care of in an hotel, and, 
according to the information obtained, his state did not differ 
from that seen under observation. 

He was admitted to M'Lean Hospital on February 9th, 1902. 
At the hospital, where he remained until his death on March 
4th, the patient showed on the whole a stable condition until 
three days before he died. His general behaviour may first be 
sketched. This will be followed by a description of his aphasia 
and his disorder of sight, and the result of the general physical 

The patient lay on his bed or sat in the chair, a good deal 
of the time apparently dozing, or sometimes he walked aim¬ 
lessly about the ward, frequently bumping into objects. When 
anyone entered his room he jumped up quickly, and when 
the physicians entered, usually shook their hands vigorously, 
and at once began to talk rapidly and voluminously, but his talk 
was often meaningless. He had a small vocabulary, and used 
wrong words, yet short sentences were at times quite clear and 
correct. He had great difficulty in understanding what was 
said to him. (All these traits will be brought out more 
clearly later.) His mood presented decided changes. He 
often beamed with smiles, and generally gave the impression 
of decided euphoria. At times he laughed immoderately 
without appreciable cause. Again he got irritable during the 
visits, or more often, especially with the nurses, was easily 
fussed up, and once tried to strike a patient who took some¬ 
thing from him at the table. Often he would not let the 
nurses take his temperature, once refused to undress at night, 
nevertheless he quite frequently appeared grateful and appre¬ 
ciative of what was done for him. As a rule he was tidy, but 
once defecated in his room. 



He usually found his room in the ward, but again wan¬ 
dered into other patients’ rooms. He was often unable to find 
the water-closet. When his people came he often recognised 
them. But again gave no clear evidence of knowing them. 

On two occasions he seems to have had hallucinations; 
both times he sat looking into the register, and said some¬ 
thing about people “ down there ” who were frightening him. 

At the examinations he was, as above stated, often euphoric, 
again irritable, seemed to tire very easily, and on account of these 
features, together with his evident difficulty in understanding 
spoken language, his co-operation in tests was often very poor. 
But a very striking feature was his frequent evidence of insight. 
When he could not understand or could not find his words, his 
desperate “ Oh dear,” or statements like “ I know but up here 
(pointing to head) I can’t say anything,” or his pathetic appeal 
once, “ Oh, if I only could get them out of here! Won’t you 
help me ? ” showed a certain appreciation of his defect, and 
argued strongly against any deeper degree of dementia. Some¬ 
times he cried at these times, when he spoke of his condition ; 
on the other hand, when, after desperate attempts to get a certain 
expression, he finally succeeded, he was childishly pleased. His 
speech showed no articulatory disorder. 

The following extracts from the notes will illustrate his 
condition more in detail:— 

Spoken commands .— 

(Show your tongue.) Complies. 

(Raise your right arm.) After puzzled thinking raises the 


(Raise your left arm.) Puts up right. 

(Sit back in your chair.) Straightens up. 

(Lean back in your chair.) “ What ? What it’s ? ” Then 
looks about puzzled, evidently thinking, finally leans back, 
saying, “ You mean this ? ” 

(Straighten your leg.) “ Leg ? What ? That ? (pointing to 
leg.) You mean straighten it? ” Then rubs head vigorously. 
“ This is it, worse, worse ”; he continues to rub his head, finally 
says, smiling broadly, “ Now I feel good.” 

In his daily life in the ward, according to the nurses, he 
sometimes understood and did as told, while at other times he 
seemed not to understand. On one occasion we told him re- 



peatedly about an accident which befell some friends of his, but 
he was unable to understand. 

Questions .— 

(What is your name ?) Pointing to head, “Here, can’t you 
feel ? Can’t you find ? Feel ? There, that’s what it is, see ? ” 

(What is your name ?) “ What is my name now ? ” He 

could not be made to give it 

(How old are you ?) “ What say ? Please ? Call ? What 

do youbmean ? What say ? What call it ? Say what ? ” 

(How old are you ?) “ Co ? No. I can’t tell you.” Then, 

irritably, “ You don’t tell.” 

(What is your age ?) “ What kind of work ? I can’t tell, 

she pulls me here something.” 

(Who is President of the U.S. ?) “ What’s I am ? Where 

I believe I am”; irritably: “ I don’t know auything about it. 
No, sir, I can't tell her anything about it. No, sir, can’t tell 
Something of that kind, see ? We are good, you know. We 
have got the world, you see ”; and, rubbing his head vigorously, 
“ Cut that right off, pull it off, you know. There it is, see ? 
See ? There, it’s a good question all the way. See ? See ? 
That’s all the way, you see; that’s all I can tell you, you see.” 
(laughing immoderately). Then, putting his hand to his head 
again, “ There is one thing that don’t let me carry here. I want 
something front here in a piece, put here on me.” Pointing to 
the physician : “ Say, this man, this man has got it, it something 
there that is.” 

At another interview he was asked his name. He said, “Oh, 
well, sir, I have been there. F. something.” Pulls a notebook 
from his pocket and turns the leaves, and says correctly, “ Well, 
it’s Frank, that is funny, if I should speak to you—Frank, F. 
I think it is Frank E. (correct). Well, I have been torn all to 
pieces (hand to head). But here now I am all mixed over 
again, I have been and had to had.” 

(Where are you ?) “ I do not know anything at all. I don’t 
know about these things, but if you let me know I will try. Oh, 
I want to go and rest, and then I’ll tell you ” (indicating the bed. 
closing his eyes, and turning head sideways). 

Naming of Objects .— 

(Hat.) “ Now, I want something like that.” Takes the hat 
and handles it. “ That tells you more than anything else.” 



(Handkerchief.) Looks at it intently. “ What mean ? Why, 
it’s all right. It’s something that. Let me go now, see ? ” He 
leans back, closes his eyes, saying rather despairingly, “ I can’t 
tell you anything now.” 

(Watch.) Points to it “That? Carren a gold.” (What 
is it ?) He points to the face of the watch, and says, “ 6—10, 
about call 10" (it was 12). (What is it?) “What’s this? 
Is leaf, leach.” 

(Cigar.) “ What is—oh, that—that’s a-.” Puts out his 

tongue and wets his lips, then in an irritated manner, “ Oh,” and 
eagerly, “ Hold it up a minute. I think that’s called go—go— 
here this way-.” 

(Keys.) “ I don’t know a thing. No, I can’t call it. No, 
now I have got something here. I don’t know what it is. He 
is a good man ” (not pointing to anyone). 

(Ten cent piece.) “ Coin, see ? Of some kind. We don’t 
carry that, don’t we ? That’s another kind (fumbling it). We 
have one of our own.” Then turns to the physician, “ I’ll tell 
you everything I can think, but sometimes I can’t think. You 
see I can’t reason.” Tapping his head : “ Where is something ? 
If I had something I could see in here.” 

According to the nurses he was most of the time unable to 
say what he wanted, but sometimes indicated his wish by signs. 
Thus he one day drew his finger around his neck and wrists 
when he was dressing, indicating that he wanted collar and cuffs, 
and was pleased when they were brought. On another occa¬ 
sion he pointed to his stomach and his mouth, and drew a 
square; the nurse brought him a lunch consisting of milk 
and crackers, and the patient appeared very pleased, saying, 
“ That’s it.” 

Usually he cannot be made to repeat words, but talks in 
his usual manner, but once repeated “ waiting.” For “ alliance ” 
said “ lions,” adding: “ That’s funny I can’t tell you so now. I 
can’t get any of them, I can’t peek.” 

He could not be made to write even his name; nor could he, 
as a rule, be made to copy anything, but would point to the 
different letters, miscalling them. When at one time he had, 
after much difficulty, read his name, and was told to copy it, he 
did copy the first two letters as if drawing them, and added the 
others in writing correctly, though awkwardly, and then appended 



an “m.” He noticed it was wrong and seemed worried about it, 
bat could not improve it. 

He was totally unable to read even individual letters (large 
print). Instead of reading he pointed to the individual letters, 
invariably miscalling them, and was unable to recognise them 
when they were directly shown and even named, and any written 
commands were treated in the same way and never complied 
with. Only once did he read correctly, namely when an envelope 
was shown him and he read “ Doctor.” His name in large print 
was given to him at another interview. He pointed to it and 
said, “ L—e—this would be—1—e—e—what’s that for ? To 
please you or to do anything for you—1—e—let’s see—e—1—I 
mean so as to make it look good. L—e—o—you see that 
don’t look well—to make it something—to give it some know¬ 
ledge,” etc. Finally he gave his name (which has L and e in 
it), but did not recognise it, repeated it several times, varied it, 
looked discouraged, but finally with marked pleasure said, “ That’s 
my name. I’m a L . . . that’s it.” 

In regard to his ability to know the -use of objects and to 
execute acts , it should be mentioned that he handled spoon and 
fork correctly, attended to his own toilet and put on his clothes 
in a correct manner. 

Of the physical examination the following may be mentioned: 
The eyes did not move equally, but the patient co-operated too 
poorly to examine them well. However, when he looked towards 
the left, the right eye did not move as far to the left as did the 
left. On other examinations it was noticed that when the right 
eye looked directly at the physician the left was turned outward. 
(The sister stated that the patient had been cross-eyed for ten 
years.) The pupils were normal in size, equal and even in 
outline. The right pupil did not react to light, while the left 
reacted normally. When the patient looked about, the width of 
the pupil changed. In tests for accommodation he did not 
sufficiently co-operate. The face was equally innervated. The 
tongue was protruded straight. There was no tremor of tongue, 
facial muscles, or extended fingers. There was no unsteadiness 
in walking. Both grips were equal, though not strong (co-opera¬ 
tion?). The patellar reflexes were prompt on both sides, but 
the right distinctly more so than the left. On the right side 
there was also a more active tendo Achillis reflex and a few 



rebounds of an ankle clonus. The plantar reflexes, however, 
were equal, and consisted in a downward motion of the toes and 
pulling up of legs. Sensation, so far as rough examination with 
pin pricks went, without good co-operation, seemed not interfered 

Vision .—That there was a defect of vision has been stated 
in the history. It will be remembered that one of his physicians 
wrote that, after the apoplectiform attack of January 17th, the 
patient had a disorder of sight. It was also noted above that 
the patient often bumped into objects, yet I could never assure 
myself that this tendency was greater on one side than on the 
other. It was difficult to determine the nature of this disorder, 
owing to the poor co-operation on the part of the patient. 
Sometimes he did not react to stimuli coming from either side 
until they reached the centre of the field of vision. This was 
the case when objects were brought from the lateral side of the 
field of vision, while the physician stood behind the patient, so 
that there was nothing but the object itself to attract his attention. 
But when the physician sat in front of the patient and with 
gestures made him understand that he wished him to grasp an 
object brought into his field of vision from the outside as soon 
as he saw it, it was found that he would do so on the right side 
only when the object traversed the median line, whereas on the 
left he repeatedly grasped it at an angle of from 50 to 55 degrees. 
There seemed, therefore, to exist, even on the left side, a certain 
defect, inasmuch as the patient’s attention could not be attracted 
by objects in the extreme lateral portion of his field of vision, 
while on the right side this evidently amounted to a half-sided 
defect. It was, unfortunately, impossible to get more accurate 

On March 2nd he was found leaning on his bureau; he 
seemed to have difficulty in moving, and when the nurse 
assisted him to bed he is said to have appeared frightened. 
Soon his right arm and hand began to twitch, later also his right 
leg and the right side of his face. When seen by a physician 
the twitching had almost subsided, but the right hand, which lay 
on the chest, appeared tremulous, and was at times jerked towards 
the mid-line and upward. He could lift the right arm, but not 
grip the physician’s hand. The right leg was rather flaccid, but 
not totally paralysed. He remained conscious, and spoke, but his 



speech was even more confused than it had been. The twitching 
continued for twenty hours with varying intensity, and although 
in the night, at times, both sides were implicated, it was still 
much more evident on the right side; the face, however, was but 
little affected. At the end of this time, 10.30 A.M., on March 
3rd, he became unconscious and had a general convulsion. 
He was found lying on his back with his head and eyes turned 
to the left, the latter also somewhat turned upward. Both sides 
were flaccid. Patellar reflexes equal and active. The two sides 
of the face equal. He was breathing stertorously and reacted in 
no way. While the physician was still present a second convul¬ 
sion came on; it began with flexion and inward rotation of the 
right foot, followed by a slight raising of the right leg; then the 
same motions began in the left leg. Soon the quadriceps began 
to contract violently on both sides, while at the same time both 
arms were flexed, the right more than the left, the hands became 
flexed at the wrists. There was a tetanic spasm seen in the 
affected groups of muscles, with slight shocks, which soon became 
more pronounced, and amounted to about 132 a minute (not all 
synchronous with the pulse). The right side of the face twitched. 
Finally the left side of the face and the left arm became more 
affected; the latter was held in the air, the forearm and hand 
flexed somewhat, and showing frequent quick contractions ; these 
were also seen in the left pectoralis. 

At 11.5 he had a third convulsion, and from then on they 
recurred at frequent intervals, but varied in intensity. They 
were then distinctly more marked on the left side. This con¬ 
tinued until 5.45 ajc. on the 4th, when he became comatose, the 
twitching stopped, he breathed stertorously, his face was deeply 
cyanosed, the eyes turned upward, purple blotches were seen all 
over the body. The temperature had reached 102‘8°, pulse 130, 
respirations 52. He died at 2.46 p.m. on March 4th. 

At the autopsy it was found that the left hemisphere was 
smaller than the right. The pia was thickened over the entire 
anterior portion of the brain; the thickening showing no special 
difference on the two sides, however. After hardening in formalin 
the left hemisphere appeared smaller, especially in the lateral 
diameter ; whereas in the longitudinal and vertical diameters the 
difference was much slighter. On the convexity the convolutions 
of die left side, except those over the posterior part of the hemi- 



sphere, were smaller than on the right side. The difference was 
extremely marked in the case of the first temporal convolution. 
This convolution appeared unusually narrow on the left side. 
The difference in weight of the two hemispheres amounted to 
120 grammes in favour of the right; the respective weights being 
710 and 590 grammes. On longitudinal sections the lateral 
ventricles presented no notable difference, but the left thalamus 
appeared somewhat smaller than the right. The two cerebellar 
hemispheres were the same in appearance and weight. The base 
of the brain and spinal cord presented nothing of note. 

The following regions were examined, chiefly with Nisei's 
stain and by means of Benda’s neuroglia method: both first 
frontal convolutions, both paracentral lobules, both first temporal 
convolutions, and pieces from the region of the fissura calcarina 
on either side. Later some large horizontal sections were made 
and three levels of the spinal cord examined. 

Microscopical Examination. 

The left first frontal convolution and the left paracentral 
lobule present the typical lesions of general paralysis in a pro¬ 
nounced degree. With the low power the whole cortex appears 
markedly narrower than that of the corresponding pieces from 
the right side, the cells are closer together, the general architec¬ 
ture is considerably disturbed. The blood-vessels are prominent, 
appear increased in number, and present small-cell infiltrations 
around them. 

With the high power it is seen that among the cells in the 
adventitial sheaths there are numerous typical plasma cells. 

Rod cells, such as Nissl and Alzheimer have described, are 
found in the tissue in considerable numbers. The glia shows 
marked changes, many nuclei are rather large, and well-defined 
cell bodies are often seen. 

The nerve cells show various degrees and forms of alteration. 

The changes in the corresponding regions of the right side 
are much less marked, though by no means absent. The process 
in the right first temporal convolution is of about the same 
intensity as that of the first frontal convolution and the para¬ 
central lobule of that side, whereas, in the region of the right 
calcarine fissure, the changes are very slight indeed. Here the 
disorder of the architecture is almost absent, but the glia ehows 



some changes, and some plasma cells are found in the vessel 

We find a very different picture in the left first temporal 
convolution, and in the region of the left fissura calcarina. 

The left first temporal convolution .—Even to the naked eye the 
cortex looks very narrow, and the tissue cuts less well than in a 
normal cortex. With the low power it is at once apparent that 
the architecture of the cortex is grossly disordered. Many nerve 
cells have disappeared, while there are present large, pale cells in 
considerable numbers. The blood-vessels are less conspicuous 
than in the less-affected portions of the brain, and the peri¬ 
vascular infiltrations slighter. With the high power the glia 
shows marked changes. The pale cells above mentioned have 
large, greyish-blue cell bodies of a rather compact appearance. 
The outline is either uneven, showing the beginning of more or 
less numerous processes, or the outline fades imperceptibly into 
the surrounding tissue. These cells either contain a large, pale 
nucleus, or a small, irregular one. The nuclei are very apt to 
be eccentric. In the most affected areas the vessels, as has 
already been stated, are not prominent. The cell infiltration 
with round cells and plasma cells is much less marked than in 
the less affected regions. Moreover, the vessels seem fewer in 
number, and rod cells much less frequently met with than in the 
portions of the cortex where the process was apparently more 
acute. The nerve cells show very marked alterations. The 
sections stained with Benda’s neuroglia method were not as 
successful as is desirable, since the neuroglia fibres did not stain 
as well as they should. Nevertheless these sections are in¬ 
structive, since the cell bodies of the neuroglia cells are stained 
very well, so that with the low power a very good idea may be 
obtained, not only of the marked disorder of the general archi¬ 
tecture of the cortex, but of the large number of these cells 
(Fig. 1). Fig. 2 does not give an adequate impression of the 
cells as seen with the oil-immersion lens, since an attempt was 
made to get the best general picture on the photograph, rather 
than to focus upon a special cell. In the sections many of the 
cells appear very large, presenting a homogeneous cell body, and 
often quite broad processes. In many places the cells present, at 
the periphery of the cell body or of the processes, rather coarse, 
deeply-stained fibres. In other cells the entire process is deeply 



stained, and it is impossible to clearly demarcate the fibres. 
Finally, there are cells and processes which present no differen¬ 
tiated fibres at all. Free fibres are also seen in the tissue. 
These cells are present throughout the cortex, and are also quite 
numerous in the white matter. 

The changes just described are those in the most affected 
areas. In other sections they are less pronounced, and even in 
the same section the intensity of the alteration varies in different 

Fissura calcarina .—The picture in this region does not differ 
from that just described, but here the changes appear to be more 
patchy. Fig. 3 shows that there is a more normal strip going 
horizontally through the middle of the cortex, whereas, in the 
upper and lower layers, the changes do not differ in intensity 
and character from those described in the first temporal con¬ 
volution. Fig. 4 shows the large glia cells as seen with the 
high power. On the whole there are places where the entire 
cortex is almost as much affected as in the most implicated 
parts of the first temporal convolution, but the intensity seems 
to vary rather more, and the marked destruction seems less wide¬ 

Besides the small sections, I have at my disposal some large 
horizontal sections through both halves of the brain, which sup¬ 
plement well the findings in the former. These sections take in 
the tip of the first temporal convolution and the second temporal 
convolution, and the fissura calcarina. In these large sections 
the difference between the right and the left side is quite 
apparent, even to the naked eye, inasmuch as the entire left side 
is considerably smaller than the right side. The cortex, too, 
especially that of the first and second temporal convolutions, is 
much thinner on the left than on the right side. 

On microscopical examination of the left side it is seen that 
the second temporal and, especially, the first temporal convolu¬ 
tion are more affected than any other convolution at the con¬ 
vexity of the brain. The first temporal presents a marked 
increase in glia in places, whereas the rest of the cortex is chiefly 
conspicuous by the marked perivascular infiltrations which are 
present everywhere. Quite striking are the changes in the 
fissura calcarina so far as it is struck by the section. Even with 
the low power large cells are seen, which, with the high power. 



can easily be identified as large glia cells such as we described in 
the picture obtained from the small section. This condition is 
seen especially in the first and second layer of the cortex, but 
dips down in a varying degree in different parts. The vessels 
are not prominent and the perivascular infiltrations slight 

On the right side the changes are more marked in the entire 
frontal lobe than in the temporal region and the parts behind 
this, so far as the convolutions of the convexity are concerned. 
The changes seem to be of moderate intensity as judged from 
the perivascular infiltration. At the tip of the frontal lobe 
there is a considerable area over which there is seen, especially 
in the deeper layers of the cortex, a marked growth of large glia 
cells, so that here an old process was evidently located, which, it 
is fair to assume, occurred at the same time as the other more 
pronounced alterations, namely, at the time of apoplectiform 
attacks. The finding in this region shows how difficult it is to 
judge of the distribution of the process from the small sections 
only. This applies equally when we come to consider the right 
calcarine fissure, which was free from any change in the small 
sections. In the large sections we here find a condition similar 
to, though less intense than, that on the left side, namely, a 
marked overgrowth of glia in the shape of large cells, seen more 
especially in the first and second layer, but also dipping down 
deeper in some places. The blood-vessels in this region, except 
those of the pia, are not conspicuous, and in this way this region 
also resembles that of the opposite side, and the other areas in 
which the process had been more destructive. The optic radia¬ 
tions are apparently intact. The external geniculate bodies are 
unfortunately not in the plane of the sections. 

An examination of sections from the cervical, thoracic, and 
lumbar cord revealed a bilateral degeneration of the pyramidal 
tracts of moderate degree and of the same intensity on the two 
sides. This degeneration was not present in the thoracic and 
cervical region. 


We have, therefore, a case of general paralysis which 
commenced somewhat over a year before its termination, pro¬ 
bably with a mild apoplectiform attack (“I was stupid and 
could not use my tongue ”). This was followed by an aphasic 



disorder which seems to have gradually improved. There were 
severe headaches. There seems to have been no decided evidence 
of a general mental involvement. A year after the onset the 
patient had a marked apoplectiform attack which left him in a 
condition as follows:—Probably moderate dementia, certainly 
euphoria and irritability, limited vocabulary, paraphasia, loqua¬ 
ciousness, great difficulty in understanding spoken language, 
great difficulty in reading and writing. One pupil inactive to 
light; reflexes increased on the right. Right-sided hemianopsia 
and difficulty of vision on the left side. 

At the autopsy the left hemisphere was smaller than the righb 
(difference, 120 grammes). Changes in the cortex throughout, 
more marked in the left hemisphere. Profounder changes de¬ 
noting a less active process in the left first temporal convolution 
and region of the left fissura calcarina. Some, though less ex¬ 
tensive, changes of the same character in the right calcarine 
fissure and at the tip of the right frontal convolution. Bilateral 
pyramidal degeneration in lumbar cord. 

The interpretation of this case seems to be this:—Early in 
the course there took place a fairly intense process in the left 
temporal lobe. This was later followed by another process of a 
more destructive character, again localised in the first temporal 
convolution, but also in both calcarine fissures, especially that of 
the left side. Such processes were first described by Lissauer, 
and later by Alzheimer. As is usually the case, these more in¬ 
tense processes gave rise to apoplectiform attacks with subsequent 
focal symptoms. The more generalised process in which the 
inflammatory changes were more in the foreground was also 
more marked on the left side throughout. 

The sensory aphasia finds its explanation in the changes 
situated in the first temporal convolution. The visual disorder 
is especially interesting. Though it was bilateral, the patient 
was not blind, but often bumped into objects on either side, and 
it was found by tests that on the whole right side his attention 
could not be attracted by movements of the hands or by objects; 
whereas on the left side this was difficult and could only be done 
to a limited degree, so far as extent and intensity were con¬ 
cerned, namely, only when the stimulus was expected and 
obtrusive, and even then not farther out of the direct vision than 
to about 50 or 55 degrees of the temporal side of the field. It 



is fair to assume that this disorder of sight is due to the changes 
which we could demonstrate in both calcarine fissures. 

Cask II. A man 37 years old. So far as the family history 
is concerned we find a marked psychopathic heredity. Since 
early youth abnormal traits were noticed in him: he was un¬ 
truthful, boastful, and when he grew up became very dissipated. 
In 1888 he had syphilis. 

In 1899 the patient began to lose weight, complained of 
fatigue, and at times of dizziness. At the beginning of 1900 
his normal tendency to bragging became a little more marked. 
In May 1900 he had a series of convulsions lasting for five hours. 
These left no sequels and he was not markedly worse in any 
way. Three months later (August 1900) he had another series 
of convulsions, after which one leg is said to have been paralysed, 
the other weak. (The informants could not state which side 
was the one more affected.) He also was unable to speak and 
write. This passed over in a short time. He was sent to a 
sanatorium, where he is said to have had Argyll-Robertson pupils, 
a slight paralytic speech defect, grandiose ideas, and marked in¬ 
coherence. In January, when again at home, he had convulsions 
and was unconscious for four days. This left him with weak¬ 
ness in the right arm and hand, so that he could not hold 
objects well. Subsequent to this he had occasional attacks of 
twitching in the right arm and hand, and on several occasions 
these became general. These attacks were not associated with 
loss of consciousness. This condition of paresis of the right arm 
with attacks of twitching in it persisted for four months. His 
speech at the time was thick, but he was evidently not aphasic. 
His mental condition was one of euphoria and irritability, but 
it is claimed that he often spoke intelligently and was not 
markedly weak mentally. Then, suddenly, three weeks before 
admission (middle of May 1901), he became pale and dull, and 
it was found that he was paralysed in the right arm and that he 
had lost his speech. He became “semi-conscious.” Two days 
later the right leg became paralysed. He remained speechless 
for a week. After that he was able to utter some monosyllables, 
while the paralysis of his leg improved, but not that of his arm. 
Ten days after the onset of these symptoms he had twelve con¬ 
vulsions. During three days he was unconscious. The convul- 



sions were chiefly localised on the right side. His speech was 
again totally lost. The weakness of the right arm and, to a 
lesser extent, that of the leg persisted. He is said to have been 
very irritable and at times euphoria 

The patient was at the hospital about three months. During 
this time his general mental condition as well as his aphasic 
disorder changed very little. For the sake of simplicity we may 
therefore summarise this and then speak of the other features, 
more especially of the condition of the right side, more in detail 
and in chronological order. The patient often seemed dull and 
his attention was attracted with difficulty, and he frequently 
seemed not to understand what was said to him, though at other 
times he executed some commands, but usually co-operated very 
poorly. At times he would put out his tongue when told, 
though usually he did not; once after he had correctly complied 
with this request and was then repeatedly told to take hold 
of a pencil, he finally again protruded the tongue. Again, he 
could a few times be made to attempt the naming of objects; 
often it seemed impossible to make him understand what was 
wanted. In sensory tests and tests for hemianopsia there was 
very little co-operation. 

He was unable to speak, and, as a rule, only produced sense¬ 
less syllables like “ pur pew ” when speaking spontaneously, 
though we were told that a few times, when his people were 
with him, and when he was evidently under some emotion, he 
spoke better, and on one such occasion said to his brother, as he 
was leaving, quite clearly, “I want you to stay,” again, “Good-bye, 
Willie,” or once, “ Mother ”; but these examples were quite 
isolated, and in the presence of the physician nothing like it 
was ever obtained from him. The nurse reported that on one 
occasion he sang the doxology so that the melody could be 
caught, but that the words were merely the usual sense¬ 
less syllables. Of the results obtained on the few occasions 
when it was possible to make him attempt to name objects, 
the following samples are typical. When told to name a 
watch he said clearly, “watch”; immediately afterwards for 
handkerchief, “ hatched—che—che—pil—pil—watch—watch.” 
For dollar bill, “watch—watch—you say watch—and some 
zitch—witch.” On another occasion he said for watch, 
“ wash—bosh—pur ”; for dollar bill, “ atchee—pur—pur ” ; 



for keys, “ hatchee—pur—pur—la.” Once he was able to 
give his first name, and when several ages were given he 
picked out the correct one. At other times he did not react 
to all such tests. He usually could not be made to write, not 
even with the left hand, but put the pencil down, when it was 
put in his hand, without making an attempt, or did not even 
take the pencil. But on one occasion, early in August, he 
wrote, of his own accord, his name correctly with his left 
hand, but seemed unable to write the r of Jr. A number of 
times an attempt was made to make him read. At times he 
did not react at all, at other times he produced the same sense¬ 
less syllables as in speaking, though once pronounced a few 
words, as “ and,” “ the,” “ don’t,” “ do,” correctly. 

As to his general mental condition, it may be stated that he 
had to be cared for a great deal, not only on account of the 
paresis of his right arm (to be presently described), but chiefly 
on account of his mental condition. He frequently was untidy, 
though he also often went to the chair when told to. He some¬ 
times fed himself with the left hand, again had to be fed. At 
times he had a tendency to chew insufficiently, so that his food 
had to be cut up into small pieces lest he choke. Frequently 
he was decidedly euphoric, would laugh and grin a great deal, 
make frequent attempts to speak, at times punch the physician 
playfully; but even on these apparently brighter days his co¬ 
operation was but little better, whether the commands were 
given in gestures or spoken language. Again he was very 
irritable, would even throw his dishes on the floor, or he tossed 
restlessly about the bed, getting angry when anything was done 
for him. Sometimes he cried. 

There was at no time any evidence of hemianopsia; when he 
walked about he never bumped against objects. Tests were 
quite unsatisfactory, owing to lack of co-operation. 

Besides his aphasia, the most striking condition was that 
of his right side, especially his arm. For the first ten days 
the arm was used but little, and when he could be made to 
touch the physician’s hand, he would raise his arm and, with 
a swaying and wavering motion, bring it towards the hand of 
the examiner, miss it, try again, miss it again, until he finally 
reached it. He could not be made to grip the hand. These 
ataxic motions were present whenever he was seen in this 




period. The arm or hand presented no atrophy at this time 
or later. He was able to walk well, and seemed not at all one¬ 
sided. Knee-jerks, tendo Achillis, and plantar reflexes were 
normal, and there was no difference on the two sides. The 
crema8terics were sluggish. Four days later, the reflexes were 
a little more active, but still equal The face showed no 
asymmetry at first, but five days after admission the right 
side showed distinct, though slight, paresis. The tongue was 
protruded straight, and showed no tremor. The pupils did not 
react to light; that there was normal accommodation could be 
seen by watching his eyes as he looked about (no co-operation). 
The eyes seemed freely movable, and there was no nystagmus. 
Sensory examination was quite unreliable; he paid no attention 
to pin pricks anywhere, except when pricked on the face; but 
there was no difference on the two sides. 

On June 17th the nurse reported that while walking about 
the patient suddenly appeared pale, his eyes became staring, 
and his right arm began to twitch, but he did not lose 
consciousness. When seen a few minutes later he was rather 
duller than usual; the right forearm was in constant athetoid 
motion. The arm became pronated and supinated, while the 
fingers were flexed and extended, these motions being quite slow. 
They continued for ten days almost uninterruptedly; he could 
move his arm voluntarily, and it showed the same ataxia as 
before. The reflexes were obtained with less readiness. The 
facial paresis was not altered, the tongue was protruded 

On June 27th he had two short attacks, with rapid twitching 
of the whole right side. After that the former rotatory move¬ 
ments ceased and the arm appeared more useless, the right leg 
dragged a little, the face was the same as before. 

On June 29th he became very dull, and showed some twitch- 
ings of the right arm and facial muscles of the right side, but not 
of the leg; he was found gripping the sheet tightly with the left 
hand, and groped aimlessly about when this was pulled away. 
The right arm did not fall quite limp when raised; it showed a 
slight resistance when passive motions were made, while the left 
resisted strongly. Both legs showed the same slight resistance. 
The knee-jerks were rather less active; the left rather more 
marked than the right. 



From that time on the arm improved, but the condition 
varied; he used it at times more, again less freely; sometimes 
the grip was quite strong, again the same ataxic motions were 
seen as before. The right leg was now not different from the 
left The facial paresis was unaltered, but the tongue now also 
deviated somewhat to the right On a sensory examination made 
on July 24th, on which day the co-operation was a little better, 
the reaction to pin pricks was quite prompt, and distinctly better 
on the right than on the left side. 

On July 31st he had three convulsions of short duration : in 
the first the whole body was implicated; in the two others the 
twitching was confined to the right arm and right side of face, 
while the eyes turned to the right He had lost consciousness. 
After he regained consciousness the twitchings of the right arm 
and leg continued for some time; later, only the thigh twitched, 
while he appeared a little duller than usual. This was interrupted 
by a short attack in which his whole body stiffened, and on 
August 4th he was almost stuporous for a day. The arm was 
again more useless, and fell limp when raised; the leg was less 
limp, the facial palsy more marked than it had been. He got 
brighter on August 9th. The hand was now held with fingers 
flexed, and it was somewhat difficult to overcome this flexor 
spasm. This is not mentioned in later notes. It was then that 
for the first time the knee-jerks were more marked on the right 
side, but both were exaggerated. The plantar reflex was not 
obtained on the right side, but was normal on the left. The 
paresis of the right side did not improve after this. The patellar 
reflex remained greater on the right side ; the plantar reflex on 
the right side was uncertain, though prompt on the left. There 
were occasional twitchings of the arm; little voluntary motion. 
On August 24th he became unconscious; there were marked 
convulsive motions on the right side which soon became general, 
but these lasted only a short time. A few hours later, Cheyne- 
Stokes breathing appeared, he did not regain consciousness and 
had no further convulsions ; his respirations rose to 40, tempera¬ 
ture not above 100°, pulse 140, and there were signs of con¬ 
solidation at the base of the right lung. He died on August 

At the autopsy the brain was asymmetrical, the left hemi¬ 
sphere being smaller than the right, especially in its lateral 



diameter. The pia was thickened over the entire anterior portion 
of the brain. The tissue of the left Rolandic region seemed 
softer than that of the corresponding portion of the right side, 
and decortication was more marked. No attempt was made to 
strip the pia over the entire brain. 

After formalin hardening, the left hemisphere appeared 
smaller than the right, chiefly in its lateral, to a lesser extent in 
its vertical, and to a still lesser extent in its longitudinal diameter; 
the shortening of the latter appearing only at the posterior por¬ 
tion of the hemisphere (difference 1 cm.). The right hemisphere 
weighed 647 grammes, the left 535, a difference of 112 grammes. 
On section, it was found that the left ventricle was somewhat 
dilated and extended further back than the right. 

The right cerebellar hemisphere looked somewhat smaller. 

The left internal carotid artery was smaller than the right. 

From the following regions pieces were taken, and examined 
chiefly by means of Nisei's stain and Benda’s neuroglia method: 
the left and right first frontal convolution, left and right para¬ 
central lobule, left and right anterior central convolution, left and 
right first temporal convolution, left and right angular gyrus, left 
and right calcarine fissure, and left third frontal convolution. 
Furthermore, sections from the medulla and from three levels of 
the spinal cord were examined by means of Weigert-Pal, and 
adjoining pieces of the cord and a piece from the pons were 
treated with Marchi’s method. 

On microscopic examination of the sections from the cortex, 
the most conspicuous feature is, that in certain regions, namely, 
the left paracentral, the left anterior central, the left first temporal, 
and the left angular gyrus, a band of very large glia cells is seen 
in the fifth layer and the transition zone from the fifth layer to 
the white matter. This band is wide enough to cover £ to f of 
the field when looked at with OeuL 2, Object. 3, Leitz. The 
glia cells in this region are of the same character and the appear¬ 
ance of the tissue is the same as described and illustrated in 
Case I. The cells are again best seen in Benda preparations, 
in which the cell bodies are very prominent. The width of 
this band of glia overgrowth is about the same in the different 
regions mentioned; and in all of them, exoept in the paracentral 
lobule, the profound alterations are seen, in places, to extend 
further up into the cortex. In the fissura calcarina of the left 



side a similar, but much smaller, band is seen. In all the other 
pieces, namely, all those taken from the right side as well as in 
the left first frontal and left third frontal convolution, there may 
be found fair-sized glia cells, but neither are they of the size, nor 
do they occur in such numbers as in the regions described. The 
difference is very striking with the low power. In Nissl sections 
these large glia cells are also quite prominent. 

Apart from this glia overgrowth, we find almost everywhere 
in the cortex the typical alterations of general paralysis, viz. 
disorders in the architecture, perivascular infiltration with 
lymphoid cells and typical plasma cells, progressive and regres¬ 
sive changes in the neuroglia cells, new formation of blood¬ 
vessels, and the existence of more or less numerous rod cells. 
But the changes are not everywhere of the same intensity. 
In the first place, the perivascular infiltration, especially that 
about the larger vessels, is throughout more conspicuous in the 
sections taken from the right hemisphere than in those taken 
from the left, at least so far as the anterior central, paracentral, 
first temporal convolution and angular gyrus are concerned. The 
first frontal convolutions on the two sides present in this, as well 
as in every other way, the same picture. The calcarine fissure 
also takes a separate place, inasmuch as the right side is not 
affected at all, whereas the left side shows moderate changes. 
But while, as we have just stated, the perivascular infiltration 
is greater in many places of the right side, the other tissue 
changes are rather greater on the left side. Not only do we 
here find the band of glia overgrowth already mentioned, but 
even the upper layers of the cortex show a greater disorder of 
architecture, more marked changes in the glia, and, on the whole, 
a greater number of rod cells than on the right side; and the 
cortex is thinner on the left than on the right side. 

It would appear from this, then, that while the frontal regions, 
so far as examined, are not different on the two sides, there is 
a marked difference behind the frontal regions. This shows 
itself, not only in the greater atrophy of the left hemisphere 
and the widening of the left ventricle, especially in its posterior 
part, and a shortening of the posterior part of the left hemi¬ 
sphere, but also, microscopically, in greater general tissue changes 
on the left side, and especially marked alterations in the fifth 
layer of the cortex and the transition zone to the white matter. 



Considering the marked affection of the motor area, it is 
interesting to note the changes which are found in the brain 
stem and the spinal cord. In Weigert sections there is seen 
a moderate, though easily recognisable degeneration of the left 
pyramidal tract in the medulla oblongata (level of the olives). 
In the spinal cord it is impossible to discover any definite 
degeneration in the pyramidal tracts or any difference on the 
two sides. With Marchi, on the other hand, we find degenera¬ 
tion in both pyramids in a piece from the pons and in pieces 
from the cervical, thoracic, and lumbar regions of the spinal 
cord. In the pons this Marchi degeneration is very marked on 
the left, but slight on the right side. In the cord the pronounced 
Marchi degeneration can be traced to the left direct and to the 
right crossed pyramidal tract. 


We have, therefore, a case of general paralysis, who, 
after a rather indefinite beginning, had convulsions, followed 
by transient paralysis in one leg and aphasia. After that, 
Argyll-Robertson pupil, paralytic speech defect, euphoria, grandi¬ 
ose ideas, and incoherence are noted. In January 1901 he had 
convulsions again, followed by weakness, and, later, occasional 
attacks of twitchings in the right arm. In May 1901 there was 
a greater loss of power in the right arm, and again aphasia. 
The aphasia henceforth remained practically unchanged, whereas 
the condition of the right arm underwent various changes, and at 
times the right leg and face were affected. Under observation 
the right arm presented at first ataxia, then, after a slight 
apoplectiform attack, athetoid motions. The latter ceased after 
renewed attacks and gave place to twitching, while the arm 
became more helpless. With repeated attacks of the same kind 
the weakness increased, and an increase of reflexes developed on 
the right side. The aphasia was characterised by an almost 
total inability to speak and write, and, evidently, by a marked 
interference with the understanding of spoken language; but 
there was also a marked degree of dementia. At the autopsy 
there was found a marked general paralytic process, with a 
greater involvement of the left side, and, so far as the examina¬ 
tion went, with especial involvement of the anterior central and 
first temporal convolutions and the angular gyrus, in which the 



most marked feature was a broad band of glia overgrowth in the 
deeper regions of the cortex. There was also found a Marchi 
degeneration in both motor tracts, but much more intense in that 
coming from the left hemisphere. In this case the difference 
between the more affected and less affected areas is less clean cut 
than in Case I. The same may be said in regard to some of the 
clinical symptoms. The dementia was much more advanced, 
the aphasia more difficult to interpret. But it is interesting to 
note in this connection that the third frontal convolution was 
not among the more involved areas, but that the first temporal 
and the angular gyrus presented very intense changes. Of 
interest are the ataxia and athetoid movements and the attacks 
of twitching in the right arm, which symptoms were associated 
with and preceded the more marked loss of power. 

Description or Plates. 

Fig. 1. —Section from first left temporal convolution of Case I. Benda’s 
neuroglia stain. Low power. Marked disorder of architecture. Dis¬ 
appearance of many nerve cells. Many large glia cells. Lack of pro¬ 
minence of vessels and of perivascular cell infiltration. 

Fie. 2.—Section from first left temporal convolution of Case I. x 375. 
Benda’s neuroglia stain. Showing detail of Fig. 1, especially the large 
glia cells. 

Fie. 3.—Section from region of fissura calcarina in Case I. Low power. 
Benda’s neuroglia stain. Showing similar condition as Fig. 1, but more 

Fig. 4—Section from left fissura calcarina of Case L x 375. Benda’s 
neuroglia stain. Showing detail of Fig. 3. 





(1) BEAL CORTEX. (Der Wert der myelogenetischen Felder 
der Orosshirnrinde.) Oskar Vogt, Anatom. Ameiger, Bd. 29, 
1906, p. 273. 

This paper contains a vigorous assault on Flechsig’s division of 
the cerebral cortex into forty or so different centres, according to 
the date of the myelinisation of their fibres. It is argued that 
Flechsig’s method of subdivision is inferior to that obtained by 
the study of the arrangement of the myelinated fibres in the adult 
brain. The areas of the cortex which myelinate early are those 
which in the adult are characterised by the number and large 
calibre of their fibres. The comparison of Campbell’s figures 
with the process of myelinisation in the developing brain shows 
that there is a complete parallelism between the richness of 
any region of the cortex in myelinated fibres and the date of 
the first appearance of myelinated fibres in that region. For in¬ 
stance, Campbell’s areae precentralis et postcentralis, which are dis¬ 
tinguished by their wealth in fibres, and especially by those of large 
calibre, correspond to the regions in which medullated fibres first 
appear. Similarly, a second focus of early myelinisation coincides 
with Campbell’s visuo-sensory area. Although the results of the 
myelogenetic investigation of the cortex are in this connection 
significant, there is nothing to show that the anatomical division 
of the cortex founded upon it is applicable to the adult brain ; on 
the other hand, the study of the arrangement of the myelinated 
fibres in the developed brain reveals all the peculiarities that each 
centre has acquired during the course of its development: it 
can, for example, distinguish between the structure of the precen¬ 
tral and the postcentral gyri, which was not possible from a study 
of the myelogenesis alone. Finally, as myelinisation starts in a 
certain number of foci, and spreads gradually from them, it is 
impossible to mark out such definite fields as Flechsig has 
attempted to do. 

The question, however, arises: Are there anatomical and 
functional differences between the early and late myelinating areas, 
such as Flechsig assumes in stating that the former represent the 
sense, and the latter the association centres ? There is no physio¬ 
logical proof of this, but Flechsig has urged two arguments in 
favour of it. Firstly, that the arrangement and character of the 
cells is different in the early and late myelinating areas, in that 



there is a resemblance between the cell architecture of each of the 
sense centres and that of their corresponding receptive organs. 
But this is certainly not so. Secondly, that the later myelinating 
regions—Flechsig’s association areas—do not possess any projec¬ 
tion fibres. C. Vogt, however, has shown that portions of the 
projection systems remain non-myelinated as long as there are 
portions of the cortex unmyelinated, and that those portions of 
the projection systems correspond to those in which secondary 
degeneration is found after destruction of Flechsig’s association 
centres in the adult brain. Therefore these too receive projection 
fibres. But Flechsig’s attempt at the subdivision of the cortex 
by the myelogenetic method has not been valueless, even though 
his conclusions cannot be accepted; it has indicated that this 
organ contains both higher and lower centres, though these cannot 
be classified as projection and association areas as Flechsig has 

On the other hand, there are strong indications that by a study 
of the different arrangementof the medullated fibres of the different 
parts of the cortex, areas can be mapped out that have different 
physiological functions. But the subdivision of the cortex is still 
more easily and more accurately possible by the study of the cyto- 
architecture of its gyri, as Campbell and Brodmann have shown. 

Gordon Holmes. 

(2) tnrelle Hirncentra mit besonderer Beriicksichtigang der struk- 
turellen Felder dee Cortex PalliL) Oskar Vogt, Verhandl. der 
anatom. Gesellsch., 1906, p. 74. 

For some years an attempt has been in progress in the Neuro- 
biological Institute in Berlin to divide the cerebral cortex into 
structural centres, that is, into areas which can be distinguished 
by fibre systems, or by their specific cell arrangement. Such a 
division can be made on the basis of the character and arrangement 
of the cells, of the myelinated fibres, or of the non-medullated 
fibrils, and the results obtained by the application of these different 
methods must be correlated and brought into agreement. The 
study of the cyto-architecture has been found to be the most 
simple ; by it areas of cortex are distinguished by the cell structure 
of their component layers, and by the arrangement of these layers. 
Vogt’s aim in the present paper has been to determine, in the first 
place, the relation of these structural centres of the cortex to 
the areas which can be marked out as belonging to any function ; 
and, secondly, to discover what relation structural centres bear to the 
sulci, which are our chief landmarks in anatomical localisation. His 



data as to the structural centres are obtained from Campbell and 
Brodmann’s publications, but for physiological localisation he has 
relied largely on the results of numerous experiments of his own 
on the localisation of the motor centres. It is interesting to see 
the marked similarity there is between the independently obtained 
conclusions of Brodmann and Campbell on histological localisation ; 
many of the areas outlined by them seem to coincide accurately 
at least, in the higher apes, on which the greater part of Brodmann’s 
work has been done. Further, Brodmann has succeeded, as Camp¬ 
bell had previously done, in following at least two of the centres— 
the precentral and visuo-sensory of Campbell—through a whole 
series of animals, from marsupials to man. 

Two anatomical types have been chosen, the precentral and 
the postcentral, on which to study the relation of the functional 
to the structural centres. There is an abrupt change in the type 
of cortex in man, the anthropoid apes, and the lower monkeys, at 
or near the fissure of Rolando, and the evidence is accumulating 
that these different types have different physiological properties. 
(1) Anatomical evidence: It is generally accepted that the fibres 
of the pyramidal system arise only from the precentral gyrus, 
though Vogt has found very slight degeneration in these tracts 
after lesions of the postcentral area in the lower monkeys. 
Further, the only degenerated fibres which reach the thalamus 
after destruction of the precentral area enter the nucleus in which 
the tegmental radiation ends, while those which come from the 
postcentral area enter the nucleus of termination of the fillet. 
This fact also suggests that the precentral and postcentral areas 
have different functions. (2) Physiological evidence: Vogt, by- 
using minimal currents in the orang, arrived at the same con¬ 
clusion as Sherrington and Griiubaum, viz. that all the excitable 
motor areas lie in front of the central sulcus. In the lower 
apes, too (twenty-four animals), he found that all excitable foci 
lie at least 1 mm. in front of the fissure of Rolando. Further, 
the frontal limits of the excitable limb areas correspond accurately 
to the frontal limit of Brodmann’s precentral type of cortex. 
The centres from which movements of the eyes and head, and the 
movements of mastication, can be obtained, correspond with further 
frontally situated structural centres of Brodmann. Again, in 
some of the lower apes the electrically excitable centres do not 
extend as far back as the fissure of Rolando, and in them the 
motor type of cortex has the same posterior limit. (3) Evi¬ 
dence obtained from destructive lesions: In the lower apes 
(11 animals), symptoms of palsy are obtained only after destruc¬ 
tion of the precentral gyrus, and the movements which remain 
possible are well co-ordinated, while if the post-central is 
injured no palsy is observed, but there is considerable ataxia. 



of movement. Therefore, in the case of the motor cortex at least, 
the structural areas coincide with the physiological centres. 

On examining one of the diagrams of Brodmann or of Camp¬ 
bell, it is at once apparent that many of the structural centres 
have no relation to the furrows, and that the margins of others are 
not bounded by the sulci. But Ziehen and Kiikenthal have insisted 
on the constancy of the chief sulci, and maintain that the homology 
of these sulci is possible in all placental mammals. But it is 
evident that physiological centres do not occupy analogous relations 
to possibly homologous fissures, and it is highly improbable that 
the variability in the position of analogous cortical fields to the 
furrows is to be ascribed to a wandering of the fields. It seems 
more probable that it is the position of the furrows which is 
inconstant, and that analogous and homologous cortical areas can 
be regarded as identical Gordon Holmes. 


(3) TION. (Le Oirconvolution godronnto et sea Prolongements tus- 
calleux.) Trolard, Rev. Neurol ., Oct. 30, 1906, p. 909. 

Only macroscopical dissection was used in this investigation. 
The size and relations of the fascia dentata are first described; 
posteriorly it is continuous with the fasciola cinerea, which is 
composed of both grey and white matter. It is generally believed 
that the fasciola cinerea bends round the splenium, and forms 
the induseum griseum which covers the dorsal surface of the 
corpus callosum, as well as the striae Lancisi and the taenia tecti. 
Trolard also admits that this may be so, but according to him its 
moet important components are the small portions of grey and 
white matter which lie on the ventral surface of the limbic gyrus, 
and form what he calls the gyrus sublimbicus. This can be 
traced as far forwards as the genu of the corpus callosum; here 
the grey matter disappears and the white fibres enter the septum. 
These fibres have no connection with the cingulum. 

Gordon Holmes. 


(4) Farrar, Am. Joum. of Insanity, No. 1,1906, p. 69. 

The cortex of different brains can be satisfactorily compared, 
either from the anatomical or physiological point of view, only 
by comparing approximately similar areas; and in routine patho¬ 
logical examination it is essential, not only that representative 
areas be chosen, but that in each case the same representative 
areas be selected. The author indicates, in diagrams attached to 



his paper, five areas of cortex which may be suitably selected for 
such routine examination. These include portions of the central, 
frontal, temporal, calcarine, and hippocampal gyri, but each 
laboratory will probably prefer a method of routine examination 
of its own. Gordon Holmes. 


(5) CEREBRAL HEMISP HERES . S. S. Maxwell, Joum. of 
Biol. Chem ., Vol. ii., 1906, No. 3, pp. 183-194. 

Following Loeb’s rule that chemical stimulation can be best 
brought about through the action of those substances, whose 
anions precipitate calcium, the author employed chiefly solutions 
of citrates and oxalates in his experiments. The experiments 
were performed upon the motor areas of rabbits and cats. 

If the substances were applied to the surface of the brain, 
no immediate response was obtained. Their effects were only 
noticeable after a latent period of many minutes (ten minutes 
or more). 

If one or two drops of citrate and oxalate solutions, isosmotic 
with blood serum, were injected into the brain substance by means 
of a specially constructed hypodermic needle, either no response 
or an immediate response was obtained. The subsequent examina¬ 
tion of the brain showed that the stimulation had been effective 
only when the needle had reached the white matter. 

Similar experiments were made with hypertonic solutions and 
solutions of barium chloride, and the same results were obtained. 

The author concludes that the grey matter is not irritable 
to chemical or osmotic stimulation. The stimulation which occurs 
after the application of certain substances to the surface of the 
brain is due to osmosis or diffusion taking place, which allows 
these substances to act on the white matter. The white matter 
is very irritable, and it responds very promptly to stimulation. 

Goltz has shown that the cortex is devoid of irritability 
to mechanical injury. Further, electrical stimulation is, ac¬ 
cording to Loeb, only a form of chemical stimulation, the effect 
of the current being to produce a relative increase at the 
cathode in the concentration of the calcium precipitant ions. The 
general conclusion reached is therefore that the cortex is devoid 
of irritability to all kinds of stimulation, and that the response 
which is obtained on electrical stimulation of the cortex is due 
to spreading. W. Cramer. 




(6) A Paper read before the Medical and Physical Society, St 
Thomas’s Hospital, 1906. 

Attention is drawn to the tendency to look upon skeletal muscles 
as affording evidence in regard to the state of the nervous system 
rather than as highly specialised tissues having important functions 
of their own. Certain results of recent work on muscle physiology 
are examined, and an attempt is made to bring them into line with 
practical clinical medicine. 

“ Plain unstriated muscle is composed almost entirely of un¬ 
differentiated sarcoplasm; its contraction is of the slow type, and 
its excitability is of a low order, that is to say, it cannot be stimu¬ 
lated to contract by the short isolated induction shock, but will 
respond to the galvanic current, which is a more powerful stimulus 
of longer duration. Pale striated muscle is rich in fibrillar aniso¬ 
tropic substance, and relatively poor in sarcoplasm ; its contraction 
is of the quick, sudden variety, and is easily elicited by isolated 
faradic shocks. Bed striated muscle, such as is found in the toad, 
although containing both the fibrillar and sarcoplasmic elements, 
is relatively rich in the latter; its contraction and excitability 
occupy an intermediate position between those of the other two 
varieties.” In man, no muscle is composed entirely of pale or 
entirely of red fibres; probably most of the muscles are made up 
of both kinds in varying proportions, which depend upon the kind 
of work for which the particular muscle is best adapted and most 
employed. Thus it is believed that sarcoplasm plays a great part 
in the production of tetanic contractions and in the maintenance 
of muscular tone; there is good reason to believe that red fibres 
are more numerous in those muscles which help to sustain the 
erect position of the human body, and that pale fibres predominate 
in those muscles which are concerned in quick, active movements. 

Botazzi’s theory of the “ functional duality ” of skeletal muscle 
is enunciated, viz. that “in striated muscle there are two con¬ 
tractile substances, the fibrillar and the sarcoplasmic, the former 
being characterised by its ready excitability, its quick contraction, 
and its poor resistance to various poisons, and the latter by its low 
excitability, its slow contraction, and its relatively great resistance 
to deleterious influences.” This theory is applied to certain clinical 

(1) The Reaction of Degeneration .—The skeletal muscle, which 
has been denervated, presents an early and marked diminution of 
its fibrillar substance, and a considerable development of sarco¬ 
plasm. This may explain, according to Ioteyko, the failure of the 
muscle to respond to faradic shocks, the persistence of response to 
the galvanic current, and the slow character of the contraction so 



produced — quite characteristic of sarcoplasmic contractility. 
Even a small proportion of fibres retaining their fibrillar structure 
will be sufficient to yield a response to the faradic current; this 
is not uncommon in progressive muscular atrophy and in myopathy, 
and may explain the persistence of faradic excitability and absence 
of complete reaction of degeneration. 

(2) Thomsen's Disease , or Congenital Myotonia .—It is impossible 
not to agree with Levi in thinking that the clinical features of 
this disease are identical with those of muscle in which there is 
an exalted state of sarcoplasmic activity. 

(3) Myoclonus .—An exaltation of fibrillar excitability may ac¬ 
count for the sudden sharp muscular contractions characteristic of 
this disease. 

(4) Myasthenia Gravis .—It is worthy of consideration—although 

Buzzard does not urge this as a full explanation of all the facts— 
whether the paralytic phenomena may not be due to impairment 
or degradation of sarcoplasmic excitability, probably secondary 
to some more general influence of toxic, possibly of autotoxic 
origin. A. W. Mackintosh. 


(7) r6gln6rescence de la moelle.) G. Marinesco et J. Minea, 
Nouv. Icon, de la SalpUribre, Sept.-Oct. 1906, p. 417. 

In this paper the authors describe the appearances found in the 
cords of dogs examined at periods varying from one to fifteen 
weeks after section, and also in two cases of compression of the 
spinal cord in man. Cajal’s ammonia-alcohol and silver method 
was employed for the examination, and the conditions found were 
very similar in the experimental and in the pathological con¬ 

New formation of nerve fibres occurred after the two fashions 
described both by the authors and by Cajal in peripheral nerves, viz. 
progressive growth of old fibres and multiplication by successive 
dichotomy of fibres of new formation. 

Growth takes place from both upper and lower ends, but seems 
to be more prolific from the posterior roots upwards than from 
above downwards. The new fibres are of varying calibre; some 
are myelinated, but most are not, they end in cones of growth or 
spherical terminal masses, and frequently have fusiform swellings 
on their course. 

Cells which they term “ apotrophic ” play the same important 
r61e here as they do in peripheral nerve regeneration. These are 



fusiform cells which are found in the tissue between the divided 
ends a few days after section, with a fusiform nucleus, and rich in 
chromatin granules. Sometimes they are elongated, with several 
nuclei, and may be termed “protoplasmic bands.” They have 
chemiotaxic properties, by which the young axons are attracted, 
and often actually drawn into their interior and nourished. The 
new nerve fibres extend by growing along these bands of apotrophic 
cells, and also by following the lines of the new vessels, forming a 
sort of perivascular reticulum. The course of the fibres is very 
irregular; many actually double back on themselves, and few 
succeed in crossing the cicatrix, so that in spite of the double cord 
and root regeneration, there is no functional restoration. To get 
this, it would be necessary for the proper neurons to become con¬ 
nected up as before, an event which can only occur with extreme 
rarity. J. H. Harvey Pirie. 

* PARENCHYMATOUS NEURITIS. (Contribute alio studio 
delle fini alterazioni della flbra nervosa—fenomeni de- e rige- 
neratdvi—nella neuriti parenchimatosa degenerativa speri- 
mentali.) Medea, Riv. Sper. di Fren., Vol. xxxii., Fasc. 3-4. 

Degenerative parenchymatous neuritis was produced in rabbits, 
guinea-pigs, and dogs by the injection of ether into nerves. 

At the point of injection the nerve structures disappeared, 
and after a short time only remnants of myeline and axis-cylinder 

Very little change was seen in the central stump at the end of 
thirty days, but after about a hundred and eighty days much 
atrophy of the fibres was found to have taken place. 

In the peripheral stump a true Wallerian degeneration followed 
the injection, but the author was unable to decide whether the 
degeneration of the myeline preceded _ that of the axis-cylinder 
or not. 

The cells which occupied the sheath of Schwann after the 
removal of the myeline and axis-cylinder were derived from the 
cells of the sheath of Schwann by a process of rapid proliferation, 
and he suggests that they may have acted as phagocytes in the 
removal of the debris. No leucocytes were seen within the sheath 
of Schwann. 

With regard to the regeneration of the nerve fibres, the author 
does not consider that the new fibres are derived from the pro¬ 
liferated cells of the sheath of Schwann, but he speaks of certain 



fibrils which he has seen lying amongst these cells but not 
connected with them, in tissues treated by the method of Cajal, 
as the precursors of the new fibres. The origin of these is not 

He inclines to the view that regeneration occurs as an outgrowth 
from the axis-cylinder of the central stump. R G. Rows. 

(9) IN THE COURSE OF POTT’S DISEASE. (Bur la p&thogtfnie 

des alterations m6dullaires survenant au eours du mal de Pott.) 

Italo Rossi, Arch, de Neurol., Jan. 1906. 

The first half of this paper gives an account of the different views 
that have been advanced as to the causation of the cord changes 
found in Pott’s disease. Briefly these are: Purely mechanical 
osseous pressure; inflammatory myelitis from the compression of 
the cord by caseous material; anaemia from direct compression of 
the meningeal vessels and indirect compression of those of the 
cord; oedema from obliteration of the veins and lymphatics, both 
by compression and thrombosis; myelitis by direct extension from 
the meninges; myelitis, with or without meningitis, from the action 
of tubercle toxines. In the second half four cases are described, 
all varying in character, and the author concludes that the patho¬ 
genesis of the changes likewise varies in different cases; but when 
there is pachymeningitis, as in the great majority of cases, there 
are the necessary and sufficient conditions to produce mechanically 
circulatory disturbances (ischaemia and oedema), which are capable 
alone of explaining the changes. When the pachymeningitis is 
too slight to have this effect, it becomes necessary to invoke another 
factor, viz. the toxines from the tubercular foci, acting, perhaps, 
more through the collateral inflammatory oedema which they cause 
than directly on the nervous elements. 

J. H. Harvey Pirie. 

(10) DISEASE. (Zur Pathogenese des Basedow’schen Symptomen- 
komplexes.) Hirschfeld, CerUralbl. f. Nervenheilk. u. Psych., 
Nov. 1, 1906, p. 832. 

The record is given of the case of a man, aged 36, who suffered 
from pains in the hip since November 1905. In March 1906 
there was found to be an extensive and inoperable sarcoma of the 
pelvis. In the end of April there developed a dreamy mental 
state, and slight exophthalmus, becoming gradually more marked. 



Later Graefe’s and Moebius’s symptoms appeared, also fine tremors 
in the fingers, and the pulse-rate reached 130 per minute. 
There was no palpable increase of the thyroid. These symptoms 
appeared and became extremely well marked in the course of a 
few days, and early in May the patient died. 

The sectio discovered a sarcoma of the pelvis with numerous 
metastases. In the thyroid were three white tumours, the size 
of cherry stones. The healthy part of the gland showed none of 
the special changes described by Askanazy, etc., but here and 
there within the edge of and surrounded by the tumour lay 
isolated follicles full of colloid materiaL The sympathetic nerve 
showed no changes, and the only disease discoverable upon care¬ 
ful examination of the central nervous system was one minute 
secondary growth in the cerebral cortex. 

Tiie writer has been quite unable to find any record of another 
case of secondary growths in the thyroid gland accompanied by 
Basedow’s disease, and the only ones in which primary thyroid 
tumour caused these symptoms were six collected by Ehrhardt in 
1902. John D. Comrie. 

(11) TIONS. (Die Microorganismen bei den endokraniellen otogenen 
Komplikationen.) Dr Hasslauer, Ceniralblait f. Ohrenheilkunde, 
Bd. 5, H. 1 and 2. 

Although the bacteriology of middle ear suppurations has be n 
thoroughly investigated, our knowledge of the organismal cause 
of resulting endocranial complications is exceedingly scanty. 
Infections of the lateral sinus are usually due to streptococcic 
invasion, but staphylococcus aureus and albus, pneumococcus, 
B. coli, B. pyocyaneus, and other organisms have been found. 
Extradural abscess is most frequently produced by the pneumo¬ 
coccus. The data are insufficient in cases of subdural abscess 
to come to any conclusion. In brain abscesses, in acute cases, 
the streptococcus is most frequently found, and next to it the 
diplococcus: in chronic cases several organisms are usually pre¬ 
sent The cases of meningitis where the actual pus was examined 
are too few in number to allow of any conclusion being drawn, 
but the cerebro-spinal fluid obtained by lumbar puncture has been 
examined in a large series of cases. In these diplococci, and next 
to them streptococci, are most frequently found; sometimes anae¬ 
robic bacilli are met with. In many cases the fluid is stated 
to have been sterile. Brieger has suggested as a possible explana¬ 
tion that these cases are due to toxins, or else that the organisms 
are very attenuated, therefore many authors lay more stress on 




immediate microscopic examination than on the study of cultures. 
It is generally agreed that the presence of bacteria must be 
demonstrated before a diagnosis of either purulent or tuberculous 
meningitis can be made ; but even here error may creep in— 
where a cerebral abscess has burst; while, on the other hand, 
the examination of the fluid may be negative, although a purulent 
meningitis is present. The diagnostic value of lumbar puncture 
has been very variously estimated, some authors placing the 
greatest trust in it, others being entirely sceptical. 

The same organisms, then, which cause middle ear suppura¬ 
tions, also bring about their endocranial complications, but that 
the various complications are induced only by certain organisms 
does not appear to be the case from what is stated above; other 
factors, such as the virulence of the organism and the resisting 
power of the individual, must also be considered. 

W. G. Porter. 


(12) Poynton and Holmes, Lancet, October 13, 1906, p. 982. 

This paper is divided into four parts. 

Part 7.— Introductory. The authors believe that the great 
majority of cases of chorea are rheumatic in nature,and hold that the 
disease is a direct result and not a complication of rheumatism. 
Acute rheumatism is the result of an infection by the “ diplococcus 
rheumaticus,” a conclusion borne out both by clinical and bacterio¬ 
logical evidence. Acute arthritic rheumatism has been produced 
in animals by experimental inoculation with a diplococcus isolated 
from the cerebro-spinal fluid and inflammatory exudations obtained 
from a case of acute rheumatism and chorea (Wassermann, 1899). 
In 1900, Poynton and Paine confirmed this observation, and also 
demonstrated the diplococcus in the pia and brain in a fatal case 
of chorea, and they produced choreiform movements in the rabbit 
by inoculating it with the organism, a result also observed by 
Meyer and by Beattie. 

Part II.—The Investigation. In two fatal cases of chorea of 
rheumatic origin, and also in a case of “chorea gravidarum,” they 
were successful in finding the diplococcus. From the heart blood 
of the first case, a girl of seven, they obtained a pure culture of 
the organism, which was also demonstrated in the pericardium 
and in the pia and brain, whilst experimental inoculation produced 
multiple arthritis and pericarditis in rabbits. The microscopical 
changes in the brain are described, the most important of these 
being congestion and occasional thrombosis of the vessels, especially 
the smaller arteries of the membranes and brain; cellular infiltra- 



(ion around these; small areas of necrotic softening; chromatolysis 
and other degenerative changes in the nerve cells, etc. The second 
case, that of a boy of fourteen, gave practically identical results; 
whilst in the third case, that of a pregnant female aged twenty-one, 
with no previous history of rheumatism or chorea, and who 
developed a very severe attack of chorea at the second month, the 
autopsy revealed recent vegetations on the mitral valve; and on 
microscopical examination of the brain, changes similar to those 
described above were found, the vascular changes being less, and 
the degenerative changes in the cells being much greater, than in 
the other two cases. 

Part III.—The Pathology of Chorea. In this section the 
authors discuss the nature of the disease and its relationship to 
other manifestations of rheumatism, their conclusion being that 
the causation of chorea is to be foimd in the action of bacterial 
toxins on the brain, producing vascular, inflammatory, and de¬ 
generative changes, though, whether these are due to direct local 
invasion or to a diffusion of toxins, they are not yet prepared 
to say. 

Part IV.—Chorea and Pregnancy. All the clinical points in 
this (the third) case, as in numerous other recorded cases, seem to 
show that the chorea of pregnancy is of the same nature as the 
chorea of childhood, and that it is a manifestation of acute 
rheumatism during a critical physiological period of special strain. 

These cases afford additional evidence that the “ diplococcus 
rheumatdcus ” is the infective agent in acute rheumatism. 

W. E. Carnegie Dickson. 

(13) patologia dell’ epilessia.) Guido Sala, Rivista Speriment. di 
Preniatria, 1906, Yol. xxxii., p. 488. 

The first thirteen pages of this article are taken up by a detailed 
review of the literature and a discussion of the work done as sup¬ 
porting one or the other of the two rival sets of findings: those 
in the cortex and those in Ammon’s horn. An account is then 
given of ten cases examined microscopically. The staining methods 
employed were mostly: for the blood-vessels, haemalum, haema- 
toxylin ; for the neuroglia, Weigert’s, Benda’s, and Dott’s modifica¬ 
tion of Heidenhain’s; for the nerve cell, Nissl’s and Pappenheim’s. 
The cases were all ones of essential epilepsy, not symptomatic. 

The results reached were as follows:— 

(1) In all the cases the cortex shewed changes more or less 
grave in relation with the duration and severity of the malady; 



these changes concerned the vessels, glia, and nerve cells; they 
varied closely with the degree of dementia, being most marked in 
a case of idiocy. 

(2) The changes were most marked in the ascending frontal 
and ascending parietal areas ; they were found, however, elsewhere 
in the cerebral cortex, particularly in the frontal and occipital 
lobes. Ammon’s horn, especially the convoluting grey layer, was 
also implicated, but always to a less extent. In one case, with 
idiocy, there were hypertrophied spider cells here, with long 
fibrillar prolongations that had intimate connection with neigh¬ 
bouring nerve cells. 

(3) The vascular changes were: dilatation and atrophy of the 
wall, dilatation of the perivascular lymphatic sheath, which was 
filled with a leucocytic infiltration; disseminated punctiform 
haemorrhages and larger extravasations occurred in cases that 
succumbed during any illness or epileptic attack. No case shewed 
the characteristic changes due to plasma cell accumulation, such as 
is seen in paretic dementia. 

(4) The neuroglia changes related especially to the sub-pial 
layer. A thick feltwork of fibrillae was formed, in the midst of 
which were found glia cells of average size. In the external layer 
of the cortex also there occurred a large number of glia cells, the 
robust prolongations of which reached, some to the vessel walls, 
others to the sub-pial feltwork, contributing to the formation of 
this. There were a fair number of monster glia cells also present. 
In the cases with dementia, evidences of active proliferation of the 
glia cells were seen. 

In Ammon’s horn the special feature was the number of monster 

(5) The changes in the nerve cells were extremely inconstant, 
varying from slight chromatolysis to advanced cellular degenera¬ 
tion. They are attributable less to the disease than to the mode 
of death, and similar findings may be seen in old age and many 
other conditions. The gigantic cells described by many authors, 
and attributed by them either to a functional hypertrophy in con¬ 
nection with the epileptic attacks or to a teratological condition, were 
found chiefly in the Rolandic region. The author disagrees with 
those who attribute significance to their presence, and thinks that 
they are probably merely large Betz cells. He thinks that not 
enough attention has been paid to the variation in size these may 
present in the normal brain. 

(6) In two cases a slight chronic lepto-meningitis was found; 
this was present chiefly over the Rolandic region, and was in 
relation to the more marked glia growth in the underlying cortex 
of that area. 

(7) In conclusion, the author is of opinion that none of the 



changes described are at all characteristic or specific of epilepsy, 
but may be found in many other morbid conditions, and even 
in simple senility. It is probable that they are all secondary 
to the circulatory disturbances mechanically produced by the 
attacks. In the case of epileptic idiocy, however, no doubt some 
of the changes, particularly the glia overgrowth, may be ascribed 
to defect in development. Ernest Jones. 

LEPTICS. (Nuove ricerche sulla nature dei prindpi tossici 
contenuti nel siero di sangue degli epilettid.) Carlo 
Ceni, Rivisi. Speriment. de Frentat., Oct. 1906, Yol. xxxii, 
p. 451. 

The latest results of the author’s well-known researches on this 
subject may be summarised as follows:— 

Animals immunised with epileptic blood serum that is hypo- 
toxic for man suffer no inconvenience. Animals submitted to a 
process of immunisation with the epileptic blood serum that is 
hypertoxic for man die rapidly if they are injected at once with 
half the dose necessary to protect an animal against the hypotoxic 
serum. The intoxication, however, presents nothing in common 
with the phenomena of epilepsy ; the animals suffer from a grave 
haemolytic process similar to that produced in man by injection of 
the same serum. The biologic reactions of the hypotoxic serum 
are in no sense specific. Their precipitating properties are con¬ 
stantly identical with those of normal blood serum. The 
hypertoxic serum, as a rule, behaves exactly in these respects as 
the hypotoxic one. In a few cases, however, it shewed a specific 
precipitation reaction in the presence of an antiserum prepared 
from the same serum. Ernest Jones. 


(15) FANCY. (Etude d’un cas de poliomydlite diffuse subaigue de 
la premi&re enfance.) P. Armand-Delille et G. Boudet, 
Nour. Icon, de la SalpUrikre, Sept.-Oct. 1906, p. 441. 

This case is remarkable as commencing in a child of two months, 
with death at six months. Weakness was first noticed in muscles 
of neck, then the extremities and trunk were progressively involved. 



Sensibility, as far as could be judged, remained quite intact. The 
organic functions were unaffected; there was never any rise of 
temperature; the cerebrospinal fluid showed a slight lympho¬ 
cytosis. In the cord the changes were confined to the anterior 
cornua—a simple atrophy of practically all the motor cells, with 
some neuroglial proliferation, but no vascular changes. The anterior 
roots and motor nerves were degenerated, while the muscles were 
extremely atrophied, with all the characters of a simple myelo¬ 
pathic atrophy. A short abstract is given of the few cases of this 
disease which have been recorded in children—none hitherto under 
one year. J. H. Habvey Pirie. 

(16) PORTANOE OF DIAGNOSIS. (Ponction lombaire, etc.) 

L. Laruelle (de Liege), Joum. de Neurol ., Nov. 20, 1906, 
p. 576. 

Dr Laruelle draws attention to the importance of the enumera¬ 
tion of cellular elements in the cytological diagnosis of cerebro¬ 
spinal fluid. 

He uses the counting cell, first used by Fuchs and Rosenthal, 
preferring that to the method of Widal, as being more practical 
and exact and requiring a shorter time for its performance. 

His method, requiring only microscope, mixing pipette, and 
counting cell, avoids the necessity of centrifuging and the various 
manipulations necessary in fixing and preparing films. He 
emphasises the fact that, in the grosser forms of meningeal affec¬ 
tions there is no difficulty in arriving at a conclusion from the 
mere appearance of the fluid, and that it is only in the narrow 
margin between slight meningeal affections, with a slight leuco- 
cytosis, and normal cerebro-spinal fluid containing a few cells, that 
any difficulty of diagnosis arises. 

Dr Laruelle lays down the proposition, as a result of experi¬ 
ment and more recently of a series of fifty cases, of which six were 
normal, that “ there is a pathological reaction present when the 
enumeration, repeated two or three times on a fresh liquid, gives 
an average of more than five leucocytic elements per cubic 
millimetre.” He gives two interesting examples of very early 
diagnosis by this means, where the other methods of examination 
of the fluid gave negative results, and in which surgical interference 
proved the correctness of the diagnosis, and enabled an earlier 
operation being performed than otherwise would have been 

Dr Laruelle points out, in conclusion, that the amount of 
cerebro-spinal fluid required is less than in the other method, 



a point sometimes of importance, and that the comparison of 
results by different observers is of much greater value, as regards 
the simplifying of the technique. Duncan Lorimer. 


(17) OF ITS DISEASE C. L. Dana (of New York), N.Y. Mtd. 
Joum., Oct. 6, 1906. 

The function of the cerebellum is essentially reflex and automatic; 
its activities are never attended by consciousness. Symptoms of 
cerebellar disease are conveniently divided into three groups— 

(a) those due to direct injury or irritation of the cerebellum, 

(b) those due to increased intracranial pressure causing general 
cerebral or local pontine or medullary symptoms, and (c) those 
due to sudden vascular changes or irritations leading to seizures. 

Of the individual symptoms, the most important are vertigo, 
nystagmus, constrained positions, muscular weakness, and reeling 
gait. The author refers to the symptoms produced by small 
cerebellar haemorrhages or softenings as forming the most typical 
and distinctive group of cerebellar symptoms. 

C. H. Holmes. 

ON 8EROU8 MENINGITIS. (Ueber serbse Meningitis.) Riebold, 
(18) D. mtd. Wchnschr., Nov. 15, 1906, p. 1859. 

The writer gives a brief historical account of this term used as 
long ago as 1844 by Barthen, and by Billroth in 1869, to describe 
an acute non-tubercular meningitis. It was only in 1887, how¬ 
ever, that Eichhorst clearly demonstrated the fact that cases arise 
acutely and remain serous, i.e. non-purulent, throughout their 
whole course. In 1893, Quincke, as the result of lumbar punctures, 
gave an exact description of the clinical picture. 

The present paper contains details of eight cases in which the 
symptoms generally speaking were headache, pains in the body 
and limbs, high temperature, slow pulse, unconsciousness, 
inequality of the pupils, and often loss of light reflex, vomiting, 
frequently ocular and other paralyses, usually leucocytosis in the 
blood. The most important sign is given by the spinal fluid, 
which is clear, of high pressure (200 or even 300 mm. of 
mercury), contains only a few lymphocytes, gives the albumin 
reactions, and is sterile as tested by making cultures or animal 
injections. Six of these cases recovered after an illness of some 



The writer agrees with Quincke that a case of serous meningitis 
may often be the exacerbation of a compensated chronic hydro¬ 
cephalus which is present as the result of an earlier meniugitis. 
He believes also that so far from being a rare affection, serous 
meningitis in slight degree is a very common affection, particularly 
as a complication of acute infectious diseases. He further points 
out that the serious cases are not to be distinguished from 
tubercular and purulent meningitis save by examination of the 
spinal fluid. John D. Comrie. 

(19) bulbaire chronique et progressive, d’origine dipht&ique.) 

Tinel and Siredey, Bull, et Mim. de la Soc. Mid. des Hdp. de 

Paris, Nov. 22, 1906, p. 1126. Scherb, ibid., Dec. 13, p. 1225. 

The extreme rarity of chronic progressive bulbar paralysis due to 
diphtheria is illustrated by the fact that the present case is only 
the eighth on record (v. Review of Neurol, and Psychiat., 1904, pp. 
461 and 562). 

A sailor, aged 24, was admitted to hospital with a history of 
deaf-mutism that had suddenly developed a month ago. This 
condition, which was found to be of hysterical origin, and to have 
been brought on by a debauch, yielded in a fortnight to appropriate 
treatment. Definite organic lesions, however, remained, which 
were as follows: atrophy of the tongue, with fibrillar contrac¬ 
tions ; paralysis of the larynx, with atrophy of the vocal cords; 
slight paresis of the lips and diminution of the senses of taste and 
hearing. Laryngoscopic examination showed complete paralysis of 
the dilators and of the crico-thyroid; the paralysis of the con¬ 
strictors was less marked. The voice was hoarse. The deep 
reflexes were normal, the general health was good, and sensation 
seemed everywhere intact. There was neither sugar nor albumin 
in the urine. 

The onset of these symptoms was traced to a severe attack of 
faucial and laryngeal diphtheria, requiring intubation, that had 
occurred in 1895, and was followed by paralysis of the palate and 
larynx. The patient did not receive antitoxin and had to wear 
the intubation tube for sixteen weeks. The palatal palsy lasted 
until 1901 and then gradually disappeared without leaving any 
trace. The paralysis of the larynx, on the other hand, became 
more marked. Even at the onset the voice was affected, and there 
were occasional suffocative attacks. Four years after his attack of 
diphtheria, the patient was under Lermoyez, when the mere 
rapid ascent of a staircase was enough to bring on the attacks, 
and the stridor was so loud at night that he had to be put in a 



room by himself. At that time the constrictors of the glottis 
were less affected. The voice was noted as good and not husky. 
Atrophy of the tongue was not present then, and was not noticed 
till June 1905. 

After travelling from the larynx along the nerve-trunks, the 
diphtheritic toxines probably affected the laryngeal centres in the 
medulla at the onset of the disease, and the contiguous nuclei 
subsequently became involved by a process of sclerosis or atrophy. 

J. D. Rolleston. 

( 20 ) SINUSES. (Em Fall von ausgedehnter Thrombosienwg dor 
Hirnsinus.) Wimmer, Berlin, klin. Wchnschr., Nov. 12, 1906. 

This is the record of a case of extensive and apparently non- 
infective thrombosis of the cerebral veins; the writer also refers 
to two other very similar cases. 

A man of 52 was suddenly seized, at work, with paralysis of 
the right arm, and general trembling followed by weakness in 
the right leg, and the same evening by twitching in the right 
side of the face. There was, however, during the first day no 
loss of consciousness. Convulsive attacks beginning in the right 
arm, followed by a condition of coma, lasting half an hour or 
thereabout, developed and recurred at frequent intervals, the 
patient dying at the end of four days. 

On account of the sudden onset, the Jacksonian symptoms, 
and marked signs of high pulse tension and diseased arteries, the 
case was regarded as a cortical arterial apoplexy. The sedio, 
however, showed thrombosis of all the large sinuses, and of the 
minute pial veins in many places with small hemorrhages. The 
cerebral arteries were quite unaffected. John D. Comrie. 

CHOREA GRAVIDARUM. Herbert French and H. T. Hicks, 
(21) Prod., Aug. 1906. 

Of twenty-nine consecutive cases of this disease treated in Guy’s 
Hospital, only three died. Barnes gave the mortality as 43 per 
cent, and Buist as 20 per cent., but these figures were founded on 
cases taken from different sources in literature, and would pro¬ 
bably not include mild cases with a favourable and uninteresting 
course. The majority of the patients were about twenty; only 
three were as old as thirty. Eighteen were primiparous. A 
distinct tendency to recurrence in later pregnancies was noted. 
In none of the cases that recovered did the temperature rise above 



99 s ; in all the fatal cases there was marked pyrexia. If there is no 
obvious complicating cause, a rise of temperature above 100° is of 
grave prognostic import. The severity of the choreic movements 
is of little prognostic value. Treatment is similar to that employed 
in chorea without pregnancy. Induction of labour is rarely indi¬ 
cated, for, on the one hand, the severest cases get better without 
it, and, on the other, it is too late to induce labour when pyrexia 
has set in. Moreover, induction of labour is not a specific cure 
for the condition. Henry J. Dunbar. 

(Sopra il significato e la frequenxa delle manifestazioni 
emilater&li nell’ epilessia essenziale.) Carlo Besta, Rivista 
Speriment. di Freniats., Oct. 1906, Yol. xxxii., p. 665. 

This subject is dealt with fully in a monograph of over sixty pages. 
Forty-three cases are described in detail, and are arranged in the 
following groups:— 

1. Fourteen cases of Idiopathic Epilepsy. These were abso¬ 
lutely typical cases except for one respect, the unilaterality of the 
manifestations. In three instances these were confined to one side 
throughout, and there was conjugate deviation of the eyes to that 
side; in six instances the tonic phase was confined to one side, but 
the clonic movements were general: in nine instances the mani¬ 
festations were bilateral throughout, but more marked on one side: 
in some of the latter cases the manifestations were bilateral 
throughout in some attacks, but only in the clonic stage in others. 
In all these cases there was a weakness on the corresponding side 
after the attacks ; in ten of the cases the weakness persisted in the 
face during the inter-paroxysmal periods; in seven the knee-jerk 
after the attack was increased on the one side; and in eight 
Babinski’s extensor response was present on that side only. 

2. Five cases of Unilateral Attacks, associated with signs 
of an old cerebral lesion. These correspond to Freud’s “cerebral 
paralysis without paralysis,” as there was no weakness, only signs 
such as Babinski’s, etc. These were due to a slight infantile 
hemiplegia of which the epilepsy was left as almost the only trace. 
Some cases were extremely difficult to differentiate from those in 
the first group, there being no sharp dividing line. 

3. Twenty-one cases of Bilateral Epilepsy. In the inter- 
paroxysmal periods it was found that of these, nine had unequal 
facial innervation on the two sides, four had deviation of the 
tongue, three asymmetry of the knee-jerks, nine asymmetry of the 
plantar reflexes, Babinski’s sign being present in one. In six of 



the cases the movements were far more pronounced on one 
side, always the same one, and there was conjugate deviation of the 
eyes towards that side. The post-paroxysmal phenomena included 
increase of the facial weakness in those suffering therefrom, 
asymmetry of the knee-jerks in thirteen cases, presence of Babinski’s 
sign in three cases; in two of the latter it was unilateral. The 
author concludes this section by demonstrating the impossibility 
of sharply dividing this group from the first. He considers it 
proved that the diminished cortical resistance in epilepsy affects 
one hemisphere more than the other in a large number of cases. 

4. Three cases of Traumatic Epilepsy. In one of these the 
manifestations were bilateral throughout, in another loss of con¬ 
sciousness was the first sign, and was followed by unilateral 
convulsions, thus exactly resembling the cases in group one. 

Many authors are quoted in confirmation of the above results. 
Especially striking were those of Redlich, who in 150 cases found 
asymmetry of the reflexes after the attack in over 40 per cent. 
The bearing of the observations on the pathology of epilepsy is fully 
discussed. The author favours the position taken by Marie, Fdr^, 
and others, who maintain the probable existence of an anatomical 
basis for the disease, in opposition to Binswanger, who claims that 
all the pathological changes described are secondary to the func¬ 
tional disturbance. The author, however, agrees with Binswanger 
that all the changes hitherto described are to be explained thus, 
but anticipates more exact results with the aid of finer methods of 
research. He does not discuss the possibility of the unilateral 
changes he describes being due also to functional disturbance. 

The final conclusions are summed up as follows:— 

1. In the majority of cases of epilepsy there exist indubitable 
signs of functional asymmetry in the interparoxysmal period. 
These concern the muscular strength, and the deep and superficial 

2. In many cases this asymmetry corresponds with the form 
of convulsion, as noted above under group 1. There is no constant 
relation, however, between the intensity of the asymmetrical signs 
and the variety of convulsion described in that group. The 
unilateral signs in the fit affect always the same side. 

3. The fit, of whatever variety, always has the effect of accen¬ 
tuating the above signs for a short while, and sometimes elicit them 
when not otherwise present. 

The initial cry is observed only in cases—though not in all of 
these—in which the functional asymmetry affects the right side. 

Ernest Jones. 




(23) MAL. (Beitrag zur Symptomatology des Petit Mai.) Bresler 
(of Lublinitz), Psych.-Neur. Wchnschr., Aug. 18, 1906. 

An attack of petit mal, as a rule, interrupts the occupation of the 
moment, which is resumed when the attack passes off. Bresler 
endeavoured to ascertain, in a patient with extremely numerous 
attacks, how far it was possible to continue some definite activity 
throughout the attack. The patient was told to count from one 
upwards, and in some of the attacks he continued to count 
throughout, in others he merely counted one or two additional 
numbers. The author found that after the attack the patient 
was sometimes able to name objects shown during the attack. 

C. Macfie Campbell. 


(24) EPILEPTIOUS. (Beitrag zur Lehre von Status hemiepilepticus.) 

Bernhardt, Berl. klin. Wchnschr ., Nov. 5, 1906, p. 1443. 

The writer records the case of a woman, aged 35, in whom 
epileptic seizures affecting especially the left side of the body 
appeared. The first attack came on in the night and was 
followed by some weakness of the left side. The following 
afternoon there was a typical epileptic fit, and another on the 
day succeeding. Afterwards, loss of consciousness and almost 
continual spasms on the left half of the body persisted, there 
was conjugate deviation of head and eyes to the left, and in¬ 
continence of urine and faces. Severe general fits finally 
appeared every half-hour. The right side of the skull was 
trephined, but no abscess, tumour, cyst, or other abnormality 
could be found, and two hours after the operation the patient 
died. No further change was found post-mortem. 

The writer gives a precis and bibliography of similar cases, 
some of which recovered. He refers to the difficulty of dis¬ 
tinguishing such cases from cerebral tumours, but mentions that 
mere trephining is sometimes remedial. 

John D. Comrie. 


(25) OF EPILEPTICS. (Die Beziehuugen der Bromwirkung zum 
Stoffwechsel der Epileptiker.) J. Hoppe, Neurolog. Centralbl ., 
Nov. 1, 1906, S. 993. 

This paper is an exposition of the principles underlying the 
Toulouse-Richet treatment. The author first refers to Landen- 



heimer’s researches, which shewed that no therapeutic results 
followed bromide administration until an equilibrium is estab¬ 
lished between its intake and excretion; this occurs only after 
the body is saturated by the accumulation of a certain amount of 
bromide, for which the giving of thirty grams is necessary. These 
researches have since, however, been supplemented. Although 
their principle has been established, it has been shewn that 
Landenheimer over-estimated the percentage of bromide in 
Bromuatrium, and also failed to take into account the varying 
excretion capacity in different people. This latter point is the 
explanation why children tolerate bromide better than adults, 
because their kidneys are less damaged. The other important 
factor is the amount of salt taken in the food. No therapeutic 
results are observed until one-third of the chlorine of the blood 
serum has been replaced by a chemically equivalent amount of 
bromine. It is known that bromide accumulates in the vessels, 
chiefly in the blood serum, and not in the organs of the body. 
When more than this amount of chlorine is displaced, intoxication 
is liable to occur. To determine when this point has been reached, 
one may examine the blood serum, 25 c.c. being necessary, or, more 
conveniently, the gastric juice, for it has been shown that the same 
rule applies here also. Now, clearly, when less chloride is taken 
in the food, this saturation point is reached sooner. For instance, 
it takes three to four weeks to reach it on an unrestricted diet, but 
only three to four days on a Toulouse-Richet salt-free diet. It 
follows that in the former case the administration of even four to 
six grains of bromide daily may go on for years without toxic 
symptoms, whereas in the latter they may appear after some weeks 
and quite suddenly. When this occurs the proportion of chlorine 
to bromine in the gastric juice may be only 0 09 to 0 26. This 
danger can be avoided by careful procedure and by the gradual 
introduction of the salt-free diet. Sudden changes in diet or in 
the variety of bromide employed bring about a variation in the 
chlorine-bromide proportion. Again, the effect of various diseases, 
especially the acute specific fevers, has to be noticed. In many 
of them, particularly in croupous pneumonia, salt-excretion is 
diminished, with the result that bromide retention occurs. Hence 
the lessened frequency of epileptic attacks during fevers, and also 
the increased risk to life owing to the depressant effect of the 
bromide. In other infections, such as a streptococcic, the reverse 
obtains. Ernest Jones. 



NERVE (3rd branch). C. L. Dana (of New York), Jou m. of 
Nerv. and Ment. Dis ., Sept. 1906. 

The monograph (Brain, 1905) of Head, Rivers, and Sherren con¬ 
tends that the afferent nervous system is composed of three different 
systems which conduct different forms of sensibility to the brain. 
(1) A protopathic system composed of fibres running in connection 
with the sympathetic and the vessels which furnish a low degree 
of sensibility to the skin and viscera. (2) A protopathic system 
composed of fibres running in the motor nerves which supply the 
sense of movement, of deep pressure, and appreciation of position, 
of muscles, joints, and tendons. By the protopathic system, pain, 
temperature, localisation, and position are appreciated, but not to 
a very delicate extent. (3) An epicritic system which supplies 
the skin alone and enables us to appreciate light touch, localisa¬ 
tion. and minor degrees of temperature, ranging between 22* and 
40° C. 

If this scheme were true for the trigeminal nerve, then one 
would expect that the surgical division of the nerve would leave 
at least the second form of protopathic sensibility, i.e. appreciation 
of movement, position, of deep pressure, and perhaps of extremes 
of temperature. Dana contends that while such an arrangement 
may or may not apply to the spinal nerves, it is certain that the 
central nervous system and the cranial nerves conduct sensation 
in a different way. To support the assertion, he cites actual cases, 
giving the detailed history of two. In the first case reported there 
was complete section of the inferior branch of the trigeminal nerve; 
every form of sensibility which it is possible to test was lost over 
the area supplied by this branch. In a complete paralysis of the 
seventh nerve there was no loss of deep sensibility or sense of 
position, although according to the scheme, section of the motor 
nerve should eliminate the second protopathic system. In the 
second case reported, one of hysteria major with anaesthesia of the 
trigeminus, there was absolute loss of all forms of sensibility, both 
deep and superficial; if there is a differentiation of sensibility into 
two types, it is in just such cases that one would expect to find, 
although not necessarily, dissociation of the two modalities. 

In cases where the pons and medulla are involved and striking 
dissociation of sensibility may occur (i.e. temperature, pain, and 
touch differently appreciated), the loss of the temperature sense 
may be absolute. From such cases Dana concludes that, at least 
in the central nervous system, temperature sensations, for example, 
are conducted by paths which conduct all degrees of sensation. 
The changes in the sensibility observed by the author in cases of 



cerebral hemorrhage involving the posterior segment of the internal 
capsule could not be explained by the scheme referred to. 

C. H. Holmes. 


(27) korliche Erweitenmg der Pnpillen.) Block, Deut. med. 
Wehnsehr ., Nov. 1, 1906, p. 1777. 

The writer records the case of a man who is said to possess the 
power of voluntarily widening his pupils by mental concentration 
on the subject. Two references are given (. Neurolog. Zentralbl., 
1899, Nos. 1 and 11; and Devi. Zeitschr. f. Nervenheilh., 1895, 
No. 2) to previously recorded cases of a similar nature. In the 
present case the patient, a morphinist, gazes into vacancy and 
wills that his pupils should widen, whereupon after three or four 
seconds they dilate to about one-fourth more of their previous 
width. At the same time the face reddens. He cannot volun¬ 
tarily narrow them, and the power to maintain the increased 
width lasts only about a quarter of a minute. 

John D. Comrie. 


(28) (La mydrlase hyBterique n’sxiste pas.) Ch. Sauvineau, Rev. 
Neurolog., Nov. 30, 1906. 

The author endeavours to show in this paper that functional 
affections of the pupil, especially dilatation, do not occur. Unless 
precautions are taken the diagnosis of hysteria may be made, 
though the subsequent course of events will reveal the true 
nature of the case. 

He records three cases where the question of hysteria arose, all 
of which, however, proved eventually to be organic lesions. 

Case 1. Sudden loss of sight in the right eye, the right pupil 
being slightly dilated and immobile. Consensual pupil reaction 
to light present when the left eye was illuminated, absent for the 
right eye. The only objective sign was a very slight pallor of 
the right disc. There was a history of a similar occurrence about 
three weeks previously, with a sudden return of vision. 

Diagnosis of a vascular lesion, probably haemorrhage into the 
optic nerve, was made. 

Four days later, patient regained sight in the right eye, and 
direct light reflex returned. There was still some concentric 
reduction of the right visual field. A month later the condition 
had relapsed with similar pupil changes, and eventually optic 
atrophy developed completely. 



Case 2. Complete blindness followed a traumatic injury to the 
eye. At a large hospital the diagnosis of hysterical amaurosis was 
made. On the second day was seen by the author. Nil abnormal 
in the eye or media except dilatation of pupil on the affected side 
and loss of direct light reflex, though the consensual reflex still 
remained in that eye. Prognosis of rapid atrophy of the optic 
nerve was made, and actually occurred. 

Case 3 was that of a woman who fell in the street after a fright 
from a motor car, and bruised her temporal region very severely. 
Exactly the same eye conditions resulted as in the first two cases 
and again hysteria was diagnosed by the medical attendant, but 
optic atrophy resulted. 

The author regards the eye condition, i.e. blindness, with dilata¬ 
tion and loss of the light reflex, as characteristic of organic disease, 
though a secondary atrophy does not appear for several weeks. 

The condition is not a true paralytic dilatation in which the 
pupil is immobile, though the perception of light remains and the 
consensual reflex from the healthy eye produces no contraction, 
such cases being met with in third nerve paralysis. 

In the third nerve cases the centrifugal fibres of the optic 
nerve are affected—in the cases described the centripetal fibres. 

In hysteria neither path is interfered with and so the reflex 

The author utters a word of warning against deception by such 
drugs as atropine. C. M. Hinds Howell. 


(Un cas d’ophtalmoplggie unilat&ale, totale et complete, avec 

c4citfe du m$me cdtd.) Boucuaud, Jottm. de Neurol ., Nov. 5, 

1906, p. 549. 

This is one of the rarest forms of ophthalmoplegia. The patient 
was a man aged 40, a worker in lead, with no definite history of 
syphilis. The first symptom was internal squint of the right eye, 
and the full development of the ophthalmoplegia occupied over 
two months, during which period there were two attacks of uncon¬ 
sciousness, not followed by paralysis, and headaches of increasing 
severity in the occipital region and on the right side of the head. 
All the muscles of the right eye were paralysed, and there was 
loss of reaction to light and accommodation, complete loss of sight 
and ptosis. At first the appearance of the fundus was normal, 
but later there developed well-marked optic atrophy. There was 
also loss of the sense of smell on the right side. Under treatment 
with large doses of iodide and mercury, recovery was complete as 



far as the movements of the eye were concerned, but the blindness 
persisted. The leeion was probably a syphilitic meningitis situated 
in die anterior and internal part of the middle cranial fossa in the 
region of the cavernous sinus. Henry J. Dunbar. 


(30) PARALYSIS. (Begriff und Localisation dor reflectorischen 
PnpiUenstarre.) L. Bach (Marburg), Die ophthalmologische 
Ktinik, June 22, 1906. 

This article commences by pointing out the necessity for accurately 
differentiating between a reflex paralysis of pupils, an amaurotic 
paralysis, and an absolute paralysis. The author defines a reflex 
paralysis as one in which the pupils show no reaction directly or 
indirectly to light stimuli, to reflex nervous stimuli, nor to 
psychical stimuli, but react promptly to convergence. Such a 
pupil is narrow, its width usually lying between 15 and 2 5 mm. 
He points out that it is distinguished from amaurotic paralysis by 
die difference in the width of the pupils and by the reaction to 
nerve stimuli and psychical stimuli, though in certain diseases the 
one passes over into the other and makes diagnosis impossible. 

The differentiation from a “ partial ” absolute paralysis (i.e. a 
general paresis) is fairly easy, since in this case all the movements 
will be more sluggish, the convergence reaction included, and the 
width of the pupils will be greater. 

The author, after reviewing various hypotheses as to the site 
of the pathological lesion or lesions leading to reflex pupillary 
paralysis, puts forward his own views as to the probable existence 
of an inhibitory centre for the light reflex and for pupillary dilata¬ 
tion in the distal portion of the medulla oblongata. While he 
admits that he can give no strict proof of the existence of such 
a centre, he thinks that a centre in such a position will best 
correlate the known facts on the subject. 

Leslie Paton. 


(31) OAL REFLEX (Preuve anatomique de la valour du reflexe 

paradoxal) Alfred Gordon, Rev. Neurolog., Nov. 30, 1906. 

Since his first communication on this subject in the Revue Neuro- 
logique of November 15,1904, the author has made a further series 
of observations, all of which tend to confirm his original conclusions. 
The cases he records in this communication exhibit the relation of 
the paradoxical reflex to cerebral compression, and further admit 
of definite proof in this respect from an anatomical point of view. 




He quotes two cases in full, in the first of which there was evidence 
of pressure on the right cerebral cortex, with presence of an 
exaggerated knee-jerk on the left side, and the presence of the 
paradoxical reflex. Babinski’s sign, Oppenheim’s sign and ankle 
clonus were, however, all absent. Operation was performed and 
the pressure relieved with disappearance of the reflex in question, 
which again appeared on recurrence of pressure. 

The second case exhibited an exactly similar association of 
symptoms, including the reflex due to traumatic injury to skulL 
Operation was successful and the reflex disappeared. The author 
concludes that the paradoxic reflex is an early and valuable sign 
of irritation or destruction of the pyramidal system and may appear 
before Babinski’s sign. C. M. Hinds Howell. 

BONE REFLEXES. (Reflexes osseux.) D. Noica and L. Strominger, 
(32) Rev. Neurol., November 1906. 

There is very little literature on this subject. In 1901, Ddjerine 
made mention of such reflexes; in 1903, Yon Bechterew described 
contractions of certain muscles on percussion of certain bony 
points, which he regarded as periosteal reflexes; and in 1905, 
Bertolotti and Yalobra published a study of bone reflexes in the 
lower limbs. In 1906, Strumpell drew attention to similar 
phenomena in both upper and lower extremities, which he 
considered to be aponeurotic and periosteal reflexes. 

The authors have carried out further investigations. They 
use a light percussion hammer for the arms, and a much heavier 
one for the legs. They find it necessary to strike gently, always 
using the same force; heavy blows excite general contractions, 
from which it is impossible to pick out the one required. 

Upper Extremity .—The arm is slightly flexed and pronated, 
the wrist slightly extended. Percussion on the styloid process 
of the radius causes contraction of biceps and supinator longus; 
on the styloid process of the ulna it causes contraction of the 
epitrochlear muscles. Percussion on the epicondyle causes con¬ 
traction of the deltoid, on the olecranon it causes contraction of 
the triceps. 

Lower Extremity. —(1) Dorsal decubitus, legs flexed on thighs, 
heels on the bed, knees slightly separated. Percussion on internal 
tuberosity of tibia causes adduction of knees. On the tuberosity 
or internal malleolus it causes contraction of the inner ham¬ 
string. (2) Lateral decubitus, leg flexed, tendo Achillis stretched, 
percussion on internal malleolus causes contraction of sural 
muscles; on the iliac crest it causes contraction of hamstrings. 

The authors find that in health the reflexes are constantly 



present in young subjects, that they diminish with advancing 
years, and may disappear in old age. In nervous disease these 
reflexes are exaggerated or diminished with the tendon reflexes. 

They are unable to decide whether these are bony or aponeu¬ 
rotic reflexes, but they show that they have no relation to the 
presence or absence of the sense of vibration, and so are not likely 
to be due to mechanical conduction of vibrations to the posterior 
roots along bones, as has been suggested. They are similar to the 
tendon reflexes, and require the integrity of a similar reflex arc. 

They point out, further, that percussion over the distribution of 
a sensory root causes contraction of the muscles innervated by the 
same segment D. W. Carmalt Jones. 

PARALYSIS. (Le rdllexe de Babinski dans les ictus dpilepti- 
formes et apoplectiformes de la paralysis gfenfirale.) Robert 
and Fournial, Rev. Neurol., November 1906. 

The extensor plantar reflex is extremely rare in general paralysis 
uncomplicated by any pyramidal lesion: the authors did not find 
a single definite instance in sixty-six cases. But in seven cases 
they found a transient extensor response after an epileptic or 
apoplectic seizure. 

They describe these cases in detail; all the patients were 
typical general paralytics, and in all a flexor plantar response was 
usually obtained. 

Six of these patients had epileptic attacks while under obser¬ 
vation, and after each attack an extensor plantar response was 
obtained for a period varying from two to ten days, after which 
flexion was again obtained. One patient had a fit, followed by 
a transient hemiplegia, an extensor response was present on the 
affected side for one day, after which plantar flexion was again 

Autopsies were performed in four of the cases, and showed the 
typical lesions of general paralysis. In several there were definite 
meningeal adhesions about the motor area. 

The authors conclude that the distinction between a transient 
extensor response, due to cerebral causes, and a permanent one 
due to organic cause, should be clinically recognised; and further, 
that pathologically Babinski’s sign is not confined to cases of pyra¬ 
midal degeneration, that pyramidal degeneration of a special kind 
is the rule in general paralysis, and that Babinski’s sign does not 
occur in general paralysis except as a transient phenomenon. 

D. W. Carmalt Jones. 



(34) di Babinski nolle malattia mental!.) Casillo, Ann. di 
Nevrolog ., 1906, Ann. xxiv., F. ii.-iii., p. 181. 

1. Babinski’s phenomenon is met with in various mental diseases 
which have an organic basis demonstrated anatomo-pathologically, 
viz. general paralysis of the insane, epilepsy, and idiocy. In 77 
cases of the first of these, an extensor response was obtained in 20 
(26 per cent); in 87 epileptics, 7 times (8 per cent.); in 87 of the 
last group, 4 times (4'6 per cent.). 

2. It is met with exceptionally in some of the autotoxic 
psychoses, not during the whole course of the disease, but in its 
acute stage. Its preseuce may suggest a lesion of pyramidal 
fibres as a result of the intoxication. S. A. K. Wilson, 

(35) INJECTION OF SCOPOLAMINE. (Ueber das Auftreten der 
Babinskischen Reflexes nach Skopolamin-Injektionen.) Link, 
Zettschr. /. klin. Med., Bd. 59, H. 2-4. 

In 1903, Volkmann found that an extensor response was obtained 
during the narcosis produced by injections of morphine and 
scopolamine, and his observation has frequently been corroborated 
since. Pawlow noticed an increase in the excitability of cutaneous 
reflexes in dogs after the injection of scopolamine. The author 
examined 43 patients, who had already been proved normal 
subjects from the point of view of reflectivity, while they were 
under the influence of scopolamine and morphia, and in 37 of 
these an extensor response was forthcoming. The shortest interval 
between the first injection and the occurrence of this reflex was 
2 minutes; as a general rule, it was obtainable from a quarter of 
an hour to an hour afterwards, and it often persisted for hours. 
In 14 cases it was remarked that stroking the sole of the foot 
produced an extensor response, while the prick of a pin was 
followed by a flexor one. 

Babinski’s phenomenon is not by any means an unfailing 
accompaniment of narcosis in general. On 6 occasions the author 
was able to note that an extensor response produced by the action 
of scopolamine disappeared when the patient was subsequently 
anaesthetised with chloroform. His view is that the presence of 
this reflex is the sequel to inhibition of cortical action by means of 
the scopolamine. If it be allowed that a flexor response is a 
cortical reflex, and an extensor response a spinal one, then it is 
easy to explain the occurrence of the latter in epilepsy, comatose 
states, deep sleep, etc.; and further, it can be understood how in 



some of the cases of scopolamine injection gentle stroking of the 
sole was followed by an extensor movement of the great toe, and a 
stronger stimulus (pin prick) by flexion. 

S. A. K. Wilson. 

(36) . la question de l’aphasie; l’aphasie de 1861 h 1866; essai de 

critique historique sur la gentee de la doctrine de Broca.) 

Pierre Marie, Semaine nUdicale, Nov. 28, 1906, p. 565. 

The doctrine of the specificity of the third left frontal convolution 
as the centre for spoken language is based on the first two 
autopsies performed by Broca. The two brains in question are 
preserved to this day in Dupuytren's Museum in Paris, where any¬ 
one may see them. Now, the first case was undoubtedly a typical 
motor aphasic, inasmuch as he had hemiplegia on the right side 
and could say nothing whatever beyond the syllable “ tan.” The 
pathological condition is a gross softening which has involved the 
third left frontal convolution in its posterior half, the Rolandic 
convolutions in their lower ends, the greater part of the upper 
temporal convolution, and a very considerable portion of the 
supra-marginal gyrus! 

In the second case the patient was 84 years of age and had 
difficulty in speaking. An examination of his brain shows 
absolutely no focal lesion of the third frontal convolution, but 
merely a senile atrophy of some of the gyri in that area, with 
depressions at intervals where the atrophy is more pronounced. 
This condition is far from uncommon in senile cerebra, as Ldri has 
recently emphasised. In Marie’s opinion, therefore, Broca’s second 
case is not one of aphasia at all, but almost certainly a “ lacunaire,” 
ie. a case in which numerous lacunes of cerebral disintegration 
existed in the grey matter of the great ganglia. 

Marie again directs attention to the fact that the artery 
which supplies the third frontal convolution is a small recurrent 
branch from the middle cerebral, and therefore unusually prone to 
suffer if the latter is involved at all, which explains the frequency 
with which softening of that convolution is associated with soften¬ 
ing of other perisylvian gyri. From the teleological standpoint, it 
is unlikely that a convolution with so precarious a blood supply 
should have assumed so important a role as that of being the 
centre for spoken language. The rest of the article consists of a 
most interesting historical retrospect on the teaching in neurology 
of the years succeeding 1861. It is clearly shown how deeply 
current thought was influenced by the tenets of Gall and other 
phrenologists, that the frontal lobes were the seat of the faculty 



of language, and how Broca was unable entirely to rid himself of 
the conception. The original must be consulted to follow the 
steps whereby the doctrine of the localisation of the motor speech 
centre in the third left frontal convolution—a doctrine never fully 
substantiated or maintained by Broca himself—has become an 
indispensable part of neurological teaching, although in Marie’s 
opinion it is based on absolutely erroneous conceptions. 

This opportunity may be taken to refer to the admirable 
lucidity and charming style of Professor Marie’s articles on 
aphasia. It may be said of them, as he himself says of Broca’s 
work, that they are “un module de clartd, de bonne humeur, 
d’esprit, et de courtoisie.” S. A. K. Wilson. 

(37) LEARN TO BEAD). J. Herbert Fisher, OphtiuU. Rev., 
Nov. 1905. 

Very few cases of this condition have been recorded, but probably 
many have been overlooked and treated for refractive errors. The 
patient was a girl aged six years, of normal intelligence and with 
no defect of vision for ordinary purposes. She had been trying to 
learn to read for two years but had made little progress. The 
letters became mixed up and she mistook simple words. She had 
also great difficulty in adding figures and in reading music. The 
fact that her mother’s brother was ten years of age before learning 
to read, and in adult life was said to spell abominably, indicates 
a family tendency to imperfection in development of the visual 
memory centre for words in the cortex of the left angular gyrus. 
The patient made good progress under the “ look and read ” system 
—learning to recognise words as a whole and not by their indi¬ 
vidual letters. The writer considers this the best method of 
instruction for such cases. Spelling should be taught orally, and 
the use of a typewriter might help to save blunders in spelling 
later in life. Henry J. Dunbar. 

A CASE OF TACTILE APHASIA. (A propos d’un cas d’aphasie 

(38) tactile.) M. Noica, Rev. Neurolog., Nov. 30, 1906. 

The first part of the paper consists of a review of the views held 
as to tactile aphasia by Baymond and Egger on the one hand, and 
Ddjerine on the other. The former, at a meeting of the Socidtd 
Neurologique, had showed a case of a lesion in the left hemisphere, 
as a result of which the right arm alone was involved. This 
patient, with his eyes closed, could tell, by means of the right 
hand, various attributes of different test objects, but was unable 



to give them a name. Raymond and Egger concluded that, as the 
power of tactile sensibility was not lost, the syndrome they describe 
does not depend on loss of such sensibility, and is therefore a true 
"tactile aphasia” depending on a central lesion, and is comparable 
to word-deafness. 

At the next meeting of the Society, D^jerine showed a man 
similarly affected, who exhibited exactly the same phenomena. 
Ddjerine was, however, of the opinion that there was a diminution 
in the acuity of tactile sensation in his case, and stated in his 
opinion that no man, intellectually sound, can present signs of 
“ tactile aphasia ” unless he has some disturbance of tactile sensa¬ 
tion. Claparede, though not supporting the name, supports the 
theory which Raymond and Egger hold, and believes the essential 
lesion to be a central one, affecting the association fibres between 
the centres of tactile perception and speech. 

The latter part of the paper contains an account of a case of 
traumatic ulnar nerve neuritis under Noica’s personal observation. 
This patient exhibited the same “tactile aphasia” as already 
described, but only in the third and fourth fingers, supplied, of 
course, by the injured nerve. He was readily able to name any 
test object placed in contact with the remaining portion of his 

The fault in this case was obviously not central but peripheral, 
and supports Ddjerine’s views on the subject. 

C. M. Hinds Howell. 


OCCUPATION PSYCHOSES. (Berufepeychosen.) W. Hellpach 
(39) (of Karlsruhe), Psyeh.-Neur. Wchnschr., July 21,28, Aug. 4,1906. 

General considerations on the peculiar mentality developed by 
or shown in certain occupations. The author thinks that the 
collector, with his hobby warping his mental activity, has a close 
affinity with the litigiously insane (Querulanten). Hysteria 
dominates the occupation psychosis, or psychopathy, of the actor; 
this profession involves the abrupt changes of mental attitude 
and of the group of dominant interests, and an unusual command 
of mimic innervation, and, as a consequence, an abnormal facility 
of discharge along these paths—an important factor in the genesis 
of hysterical complexes. Hypochondria is the special psychopathy 
of the medical profession, which involves, like the actor’s, the 
living of oneself into the life of another individual, and in addi¬ 
tion, the introspective analysis of one’s own abnormal instincts 
as a guide to those of others, and the ability to see in the earliest 
symptoms the first signs of developing disease. 



Mental disorders depend on the two factors, constitution and 
environment, and the nature of a the latter, due to a special occupa¬ 
tion,-may be the upsetting factor; with our knowledge of the 
constitution of a person, certain occupations may be looked on 
as involving certain dangers from the psychopathic point of view. 

C. Macfik Campbell. 


(40) H. A« Tomlinson (of St Peter, Minnesota), Joum. Am. Med. 

Assoc., Oct. 27, 1906. 

The author believes that the variation of muscular activity follow¬ 
ing the loss of mental capacity has been considered too little. 
Motor impulses are centrifugal and have their basis in the libera¬ 
tion in consciousness of impressions that have pre-existed and 
given rise to them. There are few forms of motion which come 
as a direct response to external stimuli. In the processes of 
degeneration the forms of motor activity involved in the most 
abstract forms of expression are the first to be lost, and the failure 
shows itself in the co-ordinate^ movements which are last in the 
order of development. When mental reduction proceeds until 
memory and attention are involved, there is commonly some evi¬ 
dence of relaxation in the normal tension of the facial muscles and 
the muscles of the eyeball; next the finer movements of hand and 
arm are affected, and this is commonly as far as the degenerative 
changes go unless mental reduction becomes extreme. These 
degenerative changes are somewhat similar in senility and in 
dementia, but the paresis of dementia is commonly spastic, while 
in senility it takes the form of tremor. Finally, the author believes 
that, where the motor activities are involved in the order of their 
development and follow this order, the change will be a permanent 
one. When this order is departed from and is not symmetrical 
and progressive, there is a probability that the power will return 
more or less completely. C. H. Holmes. 

ON SO-OALLED MORAL INSANITY. (Einige Punkte aus der 

(41) Lehre der sogenannten "Moral Insanity.”) P. Nacke (of 

Hubertusburg), Psych.-Neur. Wchnschr., June 23, 30, 1906. 

The author takes exception to the views of the Italian school, 
which makes in the group of habitual criminals a large sub-group 
of bom criminals; he holds that the born criminal is a rarity, 
and that the influence of the environment has been underrated 
by Lombroso and his followers. The habitual criminal is the 
product of a particular constitution and exogenous influences, and 



the variations in the latter form the important element in the 
majority of cases. The essence of the criminal constitution lies 
in a defect of that affective element which gives to ethical con¬ 
ceptions their dynamic value; this affective defect is closely 
connected with fundamental instincts and impulses, and in this 
connection the author makes some suggestions of anatomical 
correlation. C. Macfie Campbell. 

(42) bei Irren&rzten.) G. Lomer, Psych.-Neur. JFchnschr., Aug. 

11, 1906. 

A rather pessimistic view of the effect of the work and environ¬ 
ment on the mind of the hospital physician. Psychiatric work 
requires keen sympathy and an introspective turn of mind, which 
qualities are found only in the highly-organised individual, who 
is more susceptible than the average man to the influence of 
constant association with what is aesthetically and ethically 
abnormal. The tendency to carry the analytical and introspective 
atmosphere of the ward into one’s whole life results in a morbid 
attitude. C. Macfie Campbell. 

(43) TION. (Les ivresses ddlirantes transitoires d’origine 

alcoolique.) E. Dupr£ (of Paris) and R. Charpentier (of Paris), 
L’EnctphaU, Jan. 25, 1906. 

Two cases of transitory psychosis on the basis of acute alcoholic 
intoxication. The first case was a temperate boy of 19, worn out 
by overwork and worry, who unintentionally drank a small quantity 
of rum which had been put in a glass of beer; six hours later he 
entered the police station with a large butcher’s knife and said 
that he had just killed six Prussians in his room and that there 
remained twenty to be killed; he spent the night in the hospital, 
slept soundly, was astonished next morning to find himself in the 
hospital, had absolutely no memory of what he had 6aid on the 
previous evening. He was perfectly clear and was discharged. 

The second case was complicated by chronic alcoholism, and 
there was a history of a previous hallucinatory attack. Patient 
was a man of 40, who, after two days excessive drinking, entered 
the police station and accused himself of imaginary crimes. Next 
morning he was clear, recognised that he had talked foolishly the 
previous evening under the influence of drink, was able to be 
dischaiged. Such attacks in their onset, duration, and termina- 



tion are quite different from attacks of snb-acnte alcoholic 
delirium, on the basis of chronic alcoholism. 

C. Macfie Campbell. 

THE BLOOD PRB88URB IN PARESIS. G. L. Walton (of Boston), 
(44) Am. Med. Assoc, Oct. 27, 1906. 

From the reports of observations by Pilcz, Alexander, Craig, and 
others, the hope has been raised that in blood pressure there lies 
a practical aid in the diagnosis of paresis from other nervous 
diseases. Many more observations must be carefully made and 
tabulated before such a conclusion can be drawn. Walton 
examined 108 male patients suffering from this disease; cardiac, 
renal, and arterial disease was absent in but 44 of them. He 
arrived at the following conclusions: (1) The average blood 

pressure in paresis, taken as a whole, is high; (2) this is doubtless 
due to the prevalence of atheroma, with its cardiac and renal 
complications; (3) the average blood pressure in cases of paresis 
without atheroma, cardiac enlargement, or renal disorder, is pro¬ 
bably somewhat lower than that in health, but the variations are 
so great that it cannot be said to be uniformly low; (4) the test is 
not likely to prove of great value in the differentiation of paresis 
from other nervous disorders, though here, as elsewhere, useful in 
estimating the circulatory condition of the individual; (5) these 
observations are too few to establish a rule with regard to the blood 
pressure in varying emotional states. As far as they go, however, 
they tend to show (a) that the excited states of paresis are as 
likely to be accompanied by high as by low pressure; ( b ) that 
mental depression is accompanied by high oftener than by low 
pressure, but that it is not incompatible with low pressure; (c) 
that while the average pressure in euphoria is perhaps somewhat 
lower than in other mental states of the general paralytic, it is not 
inconsistent with high pressure, or with pronounced atheroma with 
cardiac and renal accompaniments. C. H. Holmes. 

(Ueber die Anwendung kiwstlich erzeugter venSaer HyperSmie 
des Gehirns bei Geisteskrankheiten.) Neu (of Galkhausen), 
Psych.-Neur. Wchnschr., July 7, 1906. 

Bier found that by artificially causing venous congestion of the 
brain he caused improvement in some cases of epilepsy, chorea 
minor, and headache of various origin. Neu, following Bier, has 



treated cases of mental disorders by the same method. To produce 
the congestion he applied an elastic bandage to the neck, increasing 
the pressure gradually to avoid sudden variations of blood pressure, 
and lowering the pressure of the bandage on complaint of pressure 
or heaviness in the head. The period of congestion was usually 
under twelve hours. Twenty-three cases were thus treated: general 
paralysis, 3; epilepsy, 3; melancholia (not further defined), 8; 
dementia praecox, 3; paranoia, 5 ;* amentia, 1. In no case was 
the treatment injurious to the patient; the case of amentia was 
cured. In the cases of epilepsy, dementia prsecox, and paranoia 
no improvement was observed. Some improvement was obtained 
in all the cases of melancholia. By the same treatment very 
marked relief was given to three cases of anaemic headache. The 
author does not claim more, from the small number of cases treated, 
than to show the desirability of trying this method of treatment in 
cases of mental disorder. C. Macfie Campbell. 

SCHEFFEL: HIS DISEASE (Scheffels Krankheit.) Dr P. J. 

(46) MObius. Pp. 40. Halle a. S.: Carl Marhold. 1906. Price 1 Mk. 

The first half of this pamphlet contains an account of the medical 
history of Joseph Victor Scheffel, the poet, who was born at 
Karlsruhe in 1826, and died at the age of sixty of cardio-vascular 
disease. Hereditarily burdened, dogged by ill-health from the 
age of twenty-seven, when he suffered his first cerebral attack, 
the subject of repeated relapses, culminating in his thirty-fifth 
year in one marked by delusions of persecution, a morbid sense 
of culpability and extravagant conduct; driven from place to 
place in search of health, a compulsory vagabond, his undoubted 
genius clouded by fears of a relapse, or obfuscated by alcoholic 
excess, his output of work is as remarkable as his eventual, if 
tardy, recovery, qualified though it was by a partial dementia 
which removed the poet, if it left the man. In reviewing the whole 
case, the author comes to the conclusion that Scheffel was the 
subject of dementia prsecox; but however this may be, his brief 
and necessarily fragmentary description of a deeply interesting 
personality will be of value to students of the pathography of 
genius. Dr Mobius’ brochure is in continuation of his previously 
published account of Robert Schumann, and the second half 
of the present pamphlet contains a critical appreciation of the 
former work, questioning Dr Mobius’ diagnosis, by Dr Gruhle, 
of Heidelberg, and Dr Mobius’ reply thereto. 





(47) die Indicationen der Hochgebirgskuren fiir Nervenkranke.) 

A. Nolda (St Moritz), Abhand. a. d. Geb. der N erven- und 
Geisteskrankheiten, Bd. vii., H. 3, p. 16. Halle a. S.: Carl 
Marhold. 1906. 

Apter many years spent in extensive practice in Alpine resorts 
at high altitudes, Prof. Nolda is able to speak with authority 
on the results of treatment of the neuroses at those levels. His 
material comprises over 3000 nervous cases, over 2000 of 
whom were neurasthenics, but also many cases of hysteria, 
mild melancholia, Graves’ disease, and a small number of 
epileptics. The best results, he finds, are obtained in recently 
acquired neurasthenia, the symptoms of head pain or pressure, 
sleeplessness, lassitude, and cardiac arythmia disappearing within, 
at most, fourteen days, headache and vertigo often on the first 
day. About 90 per cent, of all cases of neurasthenia are improved 
by mountain treatment. 

Heart disease, with angina pectoris, or severe myocardial 
degeneration, uncompensated valvular disease, pronounced dilata¬ 
tion, or hypertrophy, are, of course, important contra-indications; 
but he maintains, in opposition to Krafft-Ebing and Lowenfeld, 
that mild cases of “ cardiac or vaso-motor neurasthenia ” are much 
improved by removal to high altitudes. Another affection giving 
remarkably good results is that of hay-fever, about 70 per cent, 
finding immediate relief. An interesting point brought out by 
the author is that all medical treatment requires the most careful 
application at these heights, drugs of all kinds, particularly opium 
and its alkaloids, having a much more pronounced effect than 
at lower levels, and requiring exhibition in very small doses. 






F.R.C.P.E. Pp. 246. London: Macmillan and Co., Ltd. 1906. 

Price 108. 6d. net. 

The studies in clinical psychiatry which form the basis of this 
work are specially directed towards the physical disorders which 
so frequently accompany mental disease. Such physical disorders 
embrace changes in the processes of digestion, of assimilation, and 
of excretion—changes in the clinical composition of the blood, 
and in the number and relative proportion of the formed elements, 
changes in the cardio-vascular system and sometimes changes in 
various glands. In some groups of mental disorder the nature of 
the physical changes suggests the possibility of disordered meta¬ 
bolism being at the bottom of the mischief; but while hypotheses 
on this subject have been formed with great prodigality, the results 
of the workers in this field are extremely fragmentary and often 
conflicting, and do not warrant any definite conclusion as to the 
exact role played by these factors in the mental disorder. Any 
contribution to the elucidation of this question is therefore very 
welcome. Dr Bruce has in his studies paid particular attention 
to the condition of the blood and to the excretion of urea, and 
also to variations in the blood pressure. He has also made 
frequent bacteriological examinations of the blood, and has studied 
the agglutinines found in some conditions. His results are inter¬ 
esting, and must prove a stimulus towards further bacteriological 
work in psychiatry. 

In 10 cases of catatonia the blood was examined bacteriologi- 
cally “ during the acute stage ”; one case presented a pure culture 
of a short streptococcus; the serum reaction of 20 cases of catatonia 
to this organism was tested, and agglutination was obtained in 15 
cases, while 20 control serums did not give agglutination. Of 120 
cases of other forms of insanity, 12 gave agglutination; these 12 
cases were rather heterogeneous, but apparently all were condi¬ 
tions of excitement—3 cases of circular insanity, 2 of excited 
melancholia, 2 of alcoholic mania, 2 of mania with confusion in 
adolescent cases, 1 hebephrenia, 1 senile, 1 unclassified. Unfor¬ 
tunately the author does not record the clinical history of the case 
from which the organism was isolated, and does not say whether 
there was any intercurrent malady or not. He also omits any 
description of the cases which gave agglutination to this organism. 
In the absence of such absolutely necessary clinical data, this 



isolated observation cannot be utilised for any discussion of the 
nature of catatonia and its general aetiology. In the chapter on 
catatonia, the author states that in the first stage of the disease 
there is a moderate persistent hyperleucocytosis ; at the termina¬ 
tion of the acute stage, and just prior to the onset of stupor, there 
is a sharp rise in the leucocytes; on the onset of stupor, the 
leucocytes may fall, but immediately rise again, averaging between 
12,000 and 16,000 per One cannot appreciate correctly 
the value of such observations unless there is given an opportunity 
to study the clinical histories upon which the results are based, or 
unless there is some guarantee that the author is referring to some 
well-defined clinical group. The fact that under “acute melan¬ 
cholia” he gives a series of heterogeneous cases, belonging in 
reality to widely different groups, raises the question whether 
under catatonia he has not also grouped together widely dissimilar 
cases. It is certain that in the catatonic phase of a deteriorating 
psychosis, leucocytosis does not always occur. In some cases with 
leucocytosis a broncho-pneumonic attack or some other inter- 
current disease explains the leucocytosis. In any case, in 
considering the leucocytosis when present, one must keep in 
view at the same time the possibility of intercurrent disease. 
The fact that so many of the catatonics examined yielded an 
agglutinin to this organism is certainly one fact contributed 
towards the demonstration of the possibility that a catatonic 
symptom-complex may be associated with a definite toxaemia. 
Dr Bruce concludes that catatonia is an acute toxic disease with 
a definite course and onset. Such a conception is difficult to 
reconcile with what we know of the whole development of cases 
of a deteriorating psychosis which presents a catatonic phase. One 
may note that in the three cases which are given as examples of 
the psychosis the leucocytosis on admission was not above 11,000, 
and that in two cases the marked hyperleucocytosis came on 
during the period of stupor when there is a special tendency 
towards the development of broncho-pneumonic attacks, which, 
unless they are specially looked for, may easily escape attention. 

Another interesting observation from the bacteriological point 
of view is that of a woman, aged 40, who died during a second 
attack of delirium. Patient had a leucocytosis of 30,000; a 
culture from the bone marrow and from the lungs gave a pure 
growth of a coccus, while the other organs were sterile. 

It is also interesting to note that Dr Bruce found that 11 
out of 14 cases of circular insanity agglutinated an organism 
isolated from the blood of a case of excitement with confusion. 

To draw conclusions from such observations would be prema¬ 
ture, and the observations with regard to leucocytosis are frequently 
at variance with those of other workers. One must accept the 



conclusions with the greatest reserve in view of the extremely 
unsatisfactory observations of the author on his first group of 
insanities of toxic origin, viz. “ insanities the result of toxines of 
metabolic origin.” Under this group he includes (a) acute melan¬ 
cholia, (5) thyroidogenous insanity, (c) a variety of puerperal 
insanity, (d) delusional insanity, (e) chronic metabolic toxaemia 
(premature senility, chronic brain atrophy). “ Acute melancholia 
is a definite physical disease with definite physical symptoms, and 
it is a disease of adult life and the decline of life . . . the diagnosis 
depends upon the clinical symptoms—the disordered alimentary 
tract, the rapid pulse, the high arterial tension, the deficient ex¬ 
cretion of urine and urea, and the absence of hyper-leucocytosis.” 
Such symptoms do not look promising for purposes of clinical 
differentiation, and one is not surprised, under such circumstances, 
that the group of acute melancholia contains the records of cases 
belonging to absolutely different groups. Four charts are given 
to illustrate the temperature, pulse, arterial tension, and excretion 
of urea which are claimed as typical of acute melancholia, but in 
these charts the clinical symptoms upon which the diagnosis is 
said to rest are not prominent: one does not note a rapid pulse; 
there is no characteristic temperature; the high tension during a 
period of agitation is what one might expect; and the diminished 
excretion of urea is left alone to support the weight of the 
diagnosis. The first case is a typical example of the depressed 
phase of manic-depressive insanity, the essence of which is a 
simple sadness—retardation complex—and the prognosis of which 
is good for the individual attack, but with liability to the recur¬ 
rence of a similar depression, or of an “ equivalent ” manic attack 
(not merely a maniacal excitement, but an attack of a form as well 
characterised as the depression). Of the next two cases practically 
nothing but the charts is given. The fourth case presents a con¬ 
dition of hallucinatory confusion, such as frequently follows 
conditions of exhaustion, and which is different in onset, course, 
and prognosis from a case like the first. This case of hallucinatory 
confusion may with advantage be compared with a case recorded 
(p. 52) as an example of insanity of exhaustion, grouped under “in¬ 
sanities of non-toxic origin.” The case is described as depressed and 
confused; arterial tension 140 mm., T. 99, skin, as a rule, dry, 
excretion of urea not mentioned. Why is this case looked upon 
as an insanity of non-toxic origin when, in regard to the manic- 
depressive case above recorded, “the dry pigmented skin, the 
deficient excretion of urine and urea, the slightly febrile tempera¬ 
ture, unaccompanied by a hyperleucocytosis, combined with 
depression and slight confusion, are typical of a mild attack of 
metabolic toxaemia ? ” It would be superfluous to cite other 
examples to show the absurdity of classifying mental cases 



according to the present fragmentary knowledge of their disordered 
metabolism. Studies in metabolism are of great importance, but 
they must be more than mere fragments before they can be used 
for the clinical grasp of cases; and the complex conditions must 
be always kept in mind, not to mention the more elementary facts, 
such as the relation of excretion to food taken in. 

Psychiatry has made a great advance in leaving the mere 
symptomatological analysis of mental states for the better stand¬ 
point from which the onset, course, symptomatology, and outcome 
are all utilised for the appreciation of the nature of the disease ; 
order has thus been introduced into a most intricate subject by 
this method, the “ clinical method ” par excellence, which consists 
in the unprejudiced observation of each pathological phenomenon 
whatever its nature, whether it be flight of ideas or deficient ex¬ 
cretion of urea, and in the analysis not only of a transitory clinical 
picture, but of a continuous pathological process. The author 
says in the preface, “ when psychology is divorced from psychiatry, 
and the study of psychiatry is prosecuted along the lines of advance 
in general medicine, our knowledge of mental diseases cannot fail 
to be added to.” Medicine, however, has not made progress in any 
branch by neglecting to study the disordered functions of the 
special system which is its subject matter, and psychological 
phenomena are as much part of human bioldgy as the phenomena 
of nutrition. 

It is through refusing to adopt the “ clinical method ” that so 
little progress has been made of late by British psychiatry. If the 
author of these studies had followed this method, or taken advan¬ 
tage of the advances made by those who have followed it, the 
studies would have remained fragmentary, but the fragments 
would have been more easy to fit in with those provided by other 
workers for the building up of a pathology of mental diseases. 

C. Macfie Campbell. 

friederike Stelzner. Pp. 124. Berlin : S. Karger. 1906. 
Price 4 marks. 

The 200 cases dealt with in the book are all women who were 
admitted into the female division of the Psychiatric Department of 
the Charitd Hospital, Berlin, between the years 1892 and 1905. 
While the greater proportion of these cases belonged to the working 
classes, they included representatives of all social classes, as well 
as of various religious denominations and nationalities. A further 
important point in this connection is that, in addition to the fact 
that the larger number were labouring under some form of mental 



disease, there were 31 patients in whom no antecedent or subse¬ 
quent mental aberration could be discovered. The following 
classification shows the mental condition of the patients on 
examination. Melancholia, 65 cases; paranoia (acute and chronic), 
35; psychopathic constitution (degenerate), 32; without any 
apparent mental symptoms, 31; epilepsy, 11; dementia prsecox, 7; 
general paralysis, 6; alcoholism, 6 ; senile dementia, 4; imbecility, 
3; circular insanity, 1. 

The author does not profess to add anything new to the already 
extensive statistics of suicide from a demographic point of view, 
but merely to present an analysis of the cases observed, with the 
object of inquiring into—(1) the manner in which mental affec¬ 
tions conduce towards suicide; (2) the course and prognosis of 
mental affections complicated by suicidal attempts; (3) observa¬ 
tions on suicide occurring in persons of apparently sound mental 
health ; (4) the mental antecedents of persons who attempt suicide; 
(5) a discussion of the different methods of committing suicide; 
and (6) a consideration of the question of heredity as it affects 

Judged entirely from the stated objects of the book, it must be 
admitted that Dr Stelzner has succeeded in presenting, out of very 
ordinary material, some interesting and important results. The 
value of these results has been enhanced by the pains which have 
been taken to enquire into the antecedents, physical, mental, and 
social, of each patient; into the motives which actuated the 
attempt, as well as into the after-history of the cases. In the 
great majority of the cases the attempts at suicide were initiated 
and suggested by mental depression either pathological or induced 
by adverse circumstances in the surroundings. Of the 169 cases of 
mental disease, 65, or 38 per cent, were suffering from melancholia, 
but these do not exhaust the mental depressive states in the other 
forms of insanity mentioned which directly influenced the act. 
Thus, for example, all the six patients labouring under general 
paralysis attempted suicide in the depressed stage of the malady 
which is now so frequently observed. The suicidal attempt was 
the first observed symptom in 13 out of the 65 cases of melan¬ 
cholia, but the author correctly observes that that fact does not 
necessarily prove that the disease did not exist prior to the attempt. 
For, as he points out, the patients largely came from a class 
wherein the struggle for daily bread or the exigencies of social 
circumstances left little time for the observation of the slighter 
mental or physical ailments. After the shock of the attempt and 
the relaxation from other engrossing cares had broken down self- 
control and given time to think subjectively, the patients developed 
the usual agonising symptoms of the disease. A very interesting 
point is that out of 18 cases of climacteric melancholia, practically 



all recovered. This is a better prognosis than is usually given of 
this form of the disease, even in the absence of distinct attempts 
at suicide. For the treatment of degenerates who have attempted 
suicide, as well, we presume, as for all degenerates who are a 
nuisance to society, the author strongly urges the establishment of 
special forms of institution, where not only care but training and 
education of a moral nature should be given. A feature of the 
statistics which deserves notice is the small number of suicides 
due to alcohol. This is directly contrary to the opinion of some 
who hold alcohol to be one of the most active agents in developing 
the impulsive and mental attitude which leads to self-destruction. 
Of the 31 cases of suicide without any antecedent or subsequent 
symptoms of mental disease, it is interesting to note that heredity 
to suicide is not mentioned in one case. Four patients showed 
heredity to the psychoses, and 10 were the subjects of one or more 
of the milder neuroses. Suicide is generally regarded as one of 
the most hereditary conditions, and it is not a little surprising to 
find that even out of such a small number as 30 cases no direct 
heredity exists. 

Dr Stelzner has broken new ground by means of her treatment 
of the subject and by reason of the many suggestive facts she has 
been able to elucidate from an analysis of her cases. The book is 
one which everyone interested in suicide, whether from the 
clinical or the social points of view, ought to read. 

J. Macpherson. 





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• A number of references to papers on Treatment are included in the Bibliography under the 
Individual Diseases. 





■WeurolocjE anb flbs^cbiatrp 

Original articles 



Profeasor of Neurology in the University of Pennsylvania; Neurologist to 
the Philadelphia General Hospital; and Consultant to the Orthopaedic 
Hospital and Infirmary for Nervous Diseases. 

Circumscribed cortical encephalitis studied clinically, and its 
existence demonstrated by. necropsy and microscopical examina¬ 
tion, while not unique, is still so rare as to give value to the 
report of a new case. I shall not go into the history and 
literature of the subject, which is made unnecessary by the 
valuable articles of Oppenheim , 2 Hoppe,* and others. The entire 

1 Bead before the meeting of the American Neurological Association, held in 
Boston, June 4 and 5, 1906. 

1 Oppenheim, H., on “ Die Encephalitis und der Hirnabsoeas,” vol. ix. of Noth- 
nagel, “ Specielle Pathologic und Therapie,’* Wien, 1897. Oppenheim has a good 
practical article in his text-book on “Diseases of the Nervous System” on the 
different forms of acute non-purulent encephalitis. 

* Hoppe, H. H., “Acute Haemorrhagic Cortical Encephalitis,” Joum. of Ntrv. 
tad MetU. Ditease, vol. xxix., No. 9, September 1902. 

R. OF N. & P. VOL. V. NO. 2—0 



subject of non-purulent encephalitis, cortical and basilar, has 
received most attention from German writers, although a few 
excellent articles have been written by French, English, and 
American neurologists, that of Hoppe being the most elaborate 
contribution, so far as I know, of anyone writing in this 

The impulse given to the study of cortical encephalitis by 
Striimpell 1 is a good illustration of the value of the application 
of deductive reasoning in the development of exact knowledge. 
Striimpell, largely on theoretical grounds and on the basis of 
analogies, advocated the view that certain of the infantile palsies 
of children were due to a cerebral polio-encephalitis comparable 
to the polio-myelitis which had long been the well-known most 
important cause of the spinal infantile paralysis of children. 
The truth of his deduction has since been absolutely demonstrated, 
although as yet only in a limited number of cases. 

For the part played by Leichtenstern, Koenigsdorf, Schmidt, 
Eaymond, and others in the history of the subject, the reader is 
referred to the monograph and to the articles of Oppenheim and 
Hoppe above cited. 

The first case of circumscribed haemorrhagic encephalitis, 
cortical and subcortical, with necropsy and microscopical ex¬ 
amination, recorded in this country was by Dana and Schlapp 8 
before the meeting of the New York Neurological Society held 
January 2, 1900. The patient was a man sixty-seven years old, 
in whose blood the malarial plasmodium was found. After 
headache he had a hemiplegic seizure. His temperature was at 
first 104° F., but had subsequently fallen, rising again before 
death. His chief focal symptoms were left hemiplegia almost 
complete, immobility of tongue, and marked oral paresis. After 
he had been in the hospital for a week the paralysis of the arm 
and leg disappeared, but that of the tongue and lips persisted. 
No sensory symptoms were noted. An area of haemorrhagic 
softening was found in the lower portion of the post-central gyre 
and in the marginal gyres, involving mainly the deep part of the 
upper lip of the Sylvian fissure. Two or three smaller areas of 
haemorrhage were found in the centrum ovale. These were the 

1 Striimpell, A., Magdeburger Naturforsdier Vcrsammtung , Sept 22, 1884. 

a Dana, C. L., and Schlapp, M. G., Joum. of Xerv. and Ment. Disease, vol. xxvii.. 
No. 2, February 1900. 



only brain lesions, bnt the spinal cord showed two polio-myelitic 
foci, one in the upper and the other in the lower portion of the 
thoracic cord. Microscopical examination of the area of cerebral 
disease showed dilatation of blood-vessels, extravasations of blood, 
and great proliferation of cells. Small areas of softening were 
also present in the neighbourhood of the haemorrhagic extravasa¬ 
tions. The appearances closely resembled those described as 
encephalitis haemorrhagica. The case had some interesting 
features in focal symptomatology. The paralysis of the tongue 
and lips and the site of the lesion pointed to the existence of 
centres for these parts in the grey matter of the roof of the 
Sylvian fossa. Dana and Schlapp suggest that the case might 
be classed under the head of degenerative haemorrhagic en¬ 
cephalitis. Their examination of the autopsy records of sixty- 
seven cases of apoplexy showed that forty-two of them were 
haemorrhagic, eleven embolic, eleven thrombic, and three en¬ 
cephalitic. The case recorded by them is of interest in 
connection with that which will be presented in this paper, 
because of its focal motor symptomatology and the circum¬ 
scription of the lesion. Jacksonian epilepsy was not present, 
but cortical or cortico-subcortical paresis and paralysis were 
marked symptoms. 

Harlow Brooks 1 reviews the subject of acute non-suppurative 
encephalitis in an interesting manner. He believes that a 
considerable number of cases which recover are regarded as 
hysteria. The lesions of the disease are enumerated by him as : 
0) Cerebro-spinal meningitis, probably secondary to cerebritis 
and of a “ cellular type.” (2) General non-septic cerebritis 
affecting all parts of the cerebrum, and most marked in the 
cortex and particularly so in that of the motor areas. (3) 
Degeneration of many of the ganglion cells of the cortex. (4) 
Degeneration of many of the fibres arising from the large 
pyramidal cells of the cortex. (5) Diffuse degeneration affecting 
many of the fibres passing through both internal capsules. (6) 
Similar changes in the cerebellum. (7) Degeneration of many 
of the tracts of the pons and oblongata. (8) Degeneration of 
the chief descending tracts of the spinal cord. (9) Slight changes 
of the cytoplasm of the ganglion cells of the anterior horns of the 
ipinal cord, probably secondary. The symptoms which caused 
1 Brooks, Harlow, Medical New, Aug. 8, 1903, vol. lxxxiii., No. 0. 



these conditions in the case reported by Brooks were coma, 
stertorous respiration, absent patellar reflexes. The unconscious¬ 
ness persisted for three weeks. Necropsy showed no gross organic 

Cases of acute circumscribed haemorrhagic cortical encephalitis 
of the motor zone with Jacksonian epilepsy as a part of their 
symptomatology are very rare, and yet one of the first cases of 
this affection recorded had among its symptoms both cortical 
epilepsy and hemianopsia. This case was recorded by Ftlrbringer. 1 

Batten, 2 who has discussed the subject of cortical encephalitis 
in a most interesting manner, especially dwelling upon its 
relations to polio-myelitis and to encephalitis involving the basal 
nuclei, has recorded a case with necropsy in which a boy nine 
years old had aphasia of motor type and right hemiplegia, the 
eyes and head being turned to the left. Consciousness was at 
fint not lost, but the child soon became drowsy, cried out 
occasionally, and put his left arm to his head as if in pain. 
Jacksonian spasm was not present. The coma deepened and the 
patient died three days after the onset of the disease. Micro¬ 
scopical examination of the motor region showed numerous small 
haemorrhages and thromboses of the smaller vessels; but although 
this condition was most marked in the motor region of the cortex 
on the left side, it was not limited to that region. In this case, 
as in that of Ftirbringer, the affection was attributed to influenza. 

In another case without necropsy, recorded by Batten, a boy 
two and a half years old, the patient had for a time slow rhyth¬ 
mical movements of the left arm and leg. These later passed off 
and similar movements occurred in the right arm and leg, the 
latter persisting but becoming gradually less and less marked. 
Other focal symptoms were paralysis of the left external rectus, 
ataxia preventing him from walking, and intention tremor in 
the right arm and leg. The right knee-jerk was more active 
than the left; the right plantar reflex gave flexion and the left 
an extensor or Babinski response. This patient was taken ill in 
August with fever and unconsciousness which lasted for two 
days; he eventually recovered. 

It is difficult, as Batten says, to locate the lesions causing the 

1 Ftirbringer, P., Deutsch. med. Woch., No. 3, Jan. 21, 1892. 

J Batten, Fred. E., The Lancet , Dec. 20, 1902; and Tram, of the Med. Soc. of 
Load., vol. xxviii., p. 116, 190.5. 



symptoms. The encephalitis probably affected both the cerebrum 
and cerebellum as well as the sixth nerve in its course after 
leaving the nucleus. Whether the rhythmical spasm in this case 
was due to cortical motor lesions cannot be asserted. It some¬ 
times happens, as the writer has shown in another paper on 
Jacksonian epilepsy, 1 that local spasm may be due to lesions at 
the base, as in two cases of cerebello-pontile tumour recorded by 
him. The probable explanation of such cases is that they are 
caused by irritation of the pyramidal tracts when the arm and 
leg are involved, or of the facial tract or the nerve itself when 
the face takes part in the spasm. In the case of Batten, as both 
cerebellar and cranial nerve symptoms were present, the rhyth¬ 
mical movements may have been due to involvement of the 
motor tracts in the pons and oblongata; on the other hand, as 
the lesions of polio-encephalitis are often found in several or many 
parts of the brain, the motor cortex or subcortex on both sides 
may have been the seat of circumscribed foci of encephalitis. 

Spielmeyer 2 has contributed an article on the “ Symptomato¬ 
logy of Cerebral Encephalitis, especially on an Epileptic Form of 
this Affection.” This article, or a portion of it, is of considerable 
interest in connection with the case here recorded. According to 
him, either coma, paralysis, or motor excitation is always present in 
this affection. His group of epileptic cases, which is of particular 
interest here, is somewhat fully discussed. The spasms may be 
either Jacksonian or general, and are usually transient, but may 
disappear to return. I have seen several illustrations of this 
form of focal encephalitis in children in which the spasms, 
having ceased, returned, or in which they did not appear until 
some years after the attack of encephalitis, this having presented 
chiefly the features of the comatose or paralytic variety. Two 
personal cases are given by Spielmeyer showing marked en¬ 
cephalic lesion both of the cortex and subcortex of the motor 

Of interest is the view taken by Spielmeyer that the disease 
which the epileptic form of encephalitis most counterfeits is brain 
tumour. The mode of onset and progress of the two affections 

1 Mills, C. K., The Boston Medical and Surgical Journal , vol. cliv., No. 17, 
April 26,1906. 

* Spielmeyer, W., Centralblatt fUr Nervenheilkumle untl Psychiatric, vol. xxrii., 

Jute 1904. 



and the presence of optic neuritis in brain tumour furnish the 
best points of differentiation. The frequent occurrence of focal 
encephalitis in connection with infectious diseases is also a point 
of much diagnostic value. Attention is called to the resemblance 
of the symptoms of epileptic encephalitis to those of “ meningitis 
serosa,” and it is suggested that as cases of the latter affection 
have not been verified by necropsy, this form of so-called 
meningitis may be in reality an encephalitis. 

Jacksonian Spasm involving the face and arm — facio-brachial 
monoparesis—no impairment of sensation—focus of haemor¬ 
rhagic encephalitis in the motor zone, sharply delimited 
posteriorly by the central fissure. 

M. G., eighty-three years old, was a patient in the writer’s wards 
of the Philadelphia General Hospital. She had been for nearly 
three years before her admission, October 12, 1905, an inmate of 
the out-wards. Her family and past history were negative, 
except the record of some heart disease which had existed for 
about a year. The illness for which she was brought to the 
hospital began a few days before her admission. She had three 
attacks of spasm involving the left side of the face and left arm. 
She was not unconscious during the convulsive seizure, but the 
left arm became weak, especially at the wrist. 

Examination showed an old woman well nourished. Her 
tongue protruded towards the left side. The left side of the 
lower face was smoother than the right, and voluntary move¬ 
ments were not as well performed on the left as on the right. 
The movements of the upper half of the face were well performed 
on both sides, but the ocular movements were not well executed, 
either singly or together. 

The left ocular and palpebral conjunctive were greatly 
inflamed. The pupils were moderately dilated, round, and 
responded well to light, accommodation, and convergence. The 
left upper extremity showed distinct weakness in all movements 
with wrist-drop. The patient could not elevate the hand nor 
extend the fingers. Flexion of the fingers and hands was like¬ 
wise impossible, but the biceps and triceps movements and 
those of the muscles of the shoulder girdle were preserved to a 
slight degree. No paralysis was present in the lower extremity. 



Sensation was normal in the paralysed parts and also elsewhere 
throughout the body. The reflexes were normal. 

Daring the time of examination the left side of the face and 
the left hand were the seat of intermittent convulsive movements. 
The hand was drawn somewhat to the left and the angle of the 
mouth was drawn outwards and upwards. The eye was closed 
and the brow wrinkled, but without any frowning movement or 
movements of the eyeballs or jaws. Dilatation of the left nostril 
and movement of the platysma took place. In the spasm 
the movement of the hand was confined to the deep extensors of 
the fingers and thumb and group of ulnar extensors, there being 
no movement of the upper arm and shoulder muscles. 

At one time while examining the patient she had one of the 
above described convulsive attacks lasting two minutes. Con¬ 
sciousness was completely retained, and the movements were 
absent in all other parts of the body except in the arm and face 
as above mentioned. At the conclusion of this seizure the hand 
and face remained quiet for some time. These notes were made, 
October 1905, by Dr J. W. M'Connell, the assistant neurologist. 
Examination of the heart at this time showed the action of the 
heart to be irregularly intermittent; the pulse was small; a 
mitral systolic murmur was present. She was voiding very 
little urine. 

On October 15 another examination was made, showing 
almost complete loss in convergence and in moving the eyes to 
the left and in associated upward movements, although this loss 
in associated movements was more marked on the right than on 
the left. The paralysis of the left upper extremity was deeper 
than when the previous note was made. No contracture was 
present, and the lower extremity was still not involved. 

On October 16 the urine still continued to be scant, and 
she grew more apathetic and stuporous. The skin was clammy, 
and she could hardly be made to understand anything. Moist 
riles were distributed throughout the lungs. During the day 
she had six Jacksonian convulsive attacks like those already 
described. She died October 16, 1905. 

Necropsy showed the heart to be very much enlarged, all the 
cavities containing post-mortem and some ante-mortem clots. 
The musculature of the ventricles was thickened. It was 
reddish pink in colour, was soft, flabby, easily pinched through, 



and had a greasy surface. The mitral leaflet was thickened; 
the aortic leaflets were also thickened, especially the posterior. 
The aorta showed numerous patches of sclerosis, diffuse iu 
character. Several ulcers were found in the abdominal aorta 
on its posterior wall. 

The right lung was normal in size, the apex and anterior 
borders showing black pigmentation, in which areas the lung 
structure had a downy consistency. The left lung showed the 
same changes. 

The spleen was small, and the capsule stripped easily and 
presented an iced-caked appearance. It cut with some resistance. 
The surfaces were dark red in colour and presented many islands 
of fibrous tissue. 

The right and left suprarenal were normal. 

The left kidney was normal in size, flabby, and cut with 
considerable resistance; the capsule was thickened and stripped 
with difficulty, leaving a granular surface. The cortex was narrow 
at points ; medullary portion was purplish and congested. The 
pelvis contained an increased amount of fat. 

The right kidney showed changes similar to those of the left. 
Cirrhosis of the liver was present. Examination of the stomach, 
intestines, pancreas, and other organs showed nothing abnormal. 

On removing the calvarium, the meninges showed nothing 
noteworthy. A haemorrhage was present in the right parieto¬ 
occipital fissure. A pathological area, apparently to the naked 
eye one of softening, was found in the precentral convolution in 
the arm area and upper portion of the face area (Fig. 1). 

The ventricles were normal; the arteries at the base of the 
brain were hard and sclerotic. 

A section of the pons made just cephalad of the fifth nerve 
showed an area possibly abnormal, this not including the motor 
bundles, but microscopical examinations failed to confirm this 

The specimens were sent to the Laboratory of Neuropathology 
at the University of Pennsylvania, where they were examined by 
Dr Wm. G. Spiller, to whom I am indebted for the following 

The middle third of the right precentral convolution is 
distinctly softer than the surrounding tissue, and on section the 
softening is seen to be the result of numerous haemorrhages within 



the cortex. A haemorrhage of recent origin, about the size of a 
hickory nut, is in the outer portion of the right occipital lobe. 

Microscopical sections through the affected precentral convolu¬ 
tion show that the numerous minute haemorrhages are almost 
confined to the cortex, although a few are in the subjacent white 
matter. At the region of greatest extension the anterior one-fifth 
of the precentral convolution alone escapes. The haemorrhages 
extend deep into the central fissure, but do not pass beyond the 
bottom of the fissure into the post-central gyrus. The diseased 
cortex stands out very sharply to the naked eye. The transition 
from the normal to the haemorrhagic cortex is quite sharp, even 
under the microscope. The pia adjacent to the affected cortex is 
also haemorrhagic. A considerable amount of black granular 
pigment is found in the haemorrhagic cortex. Numerous fatty 
granular cells and round cells are in the pia over the haemorrhagic 
cortex. A small round haemorrhage about *5 cm. in diameter 
is found at the extreme lower end of the haemorrhagic area. 
The sharp limitation to the precentral gyrus, and the 
almost complete limitation to the cortex of this gyrus and 
to its posterior half are very striking. There is no round¬ 
cell infiltration about the chiasm, but there is slight round-cell 
infiltration about the small vessels of the cerebral peduncles 
<Kg. 2). 

The symptomatology and pathology of this case speak for them¬ 
selves in the light of the short study of the literature of the subject 
prefixed to the history. The strict limitation of the lesion to the 
cortex anterior to the bottom of the central fissure is of interest 
in connection with the question of the absolute precentral position 
of the motor zone. The disturbances of ocular movements and 
the hemianopsia apparently present were probably due to the gross 
hemorrhage in the occipital region. 




By ERNEST JONES, M.D., M.R.C.P. (Loud.), 

Assistant Physician at the London School of Clinical Medicine, 
Seamen’s Hospital, Greenwich ; 

Medical Examiner of Defective Children, London County Council Schools. 

The study of heredity in medicine is becoming increasingly 
important from both a theoretic and practical standpoint, and 
it is more and more apparent that many of the problems can 
be solved only after the accumulation of a large amount of 
suitable material. Particularly is this evident in the case 
of the affections that we may assume to be pure biological 
variations, such as occur especially in the nervous system, and 
it is therefore expedient that such cases, certainly those belonging 
to the rarer varieties, be recorded whenever an opportunity for 
investigating them presents itself. I have recently had occasion 
to examine a family in which eight cases of hereditary spastic 
paraplegia occurred in a single childship, 1 and wish here to 
publish a brief account of the family. The family, which has 
been under my observation for over a year, was shewn at a 
clinical meeting of the University College Hospital Medical 
Society in November 1905. I do not propose to refer to any 
of the extensive literature of the subject, as I hope to incor¬ 
porate a discussion of it in a later contribution on an allied 

Clinical Features. 

As the features were so similar in the different members of 
the family, I will describe only one case in detail, and then 
mention the characteristics of the other members. It may be 
taken that the description of the first case applies to the 
others in all respects, except where the contrary is expressly 

1 Term introduced by Professor Karl Pearson to signify the total offspring of a 
single onion. 



Ernest L., the second boy, aged 14, 1 is the most advanced 
case, and accordingly I select him as the type. He first came 
under my observation at the Old Kent Road Centre for Physically 
Defective Children, in November 1905. His mother had con¬ 
sidered him normal in all respects until after he began to walk, 
which he did between the ages of one and two. Shortly after 
this she noticed that his gait was becoming stiff and clumsy ; it 
was manifestly so by the age of three. About the same time 
she also began to notice that his feet were changing shape. The 
right foot was the first affected, but the left was implicated within 
a few months. The subsequent course of the disease was quite 
gradual and slowly progressive. Of late years, perhaps for three 
or four, the progress has ceased altogether, or has been so slight 
as to be inappreciable. Nothing else of importance was gleaned 
from the history. The boy thinks that he is, if anything, better 
than he was two years ago. He suffers from no symptoms beyond 
the difficulty in walking, which he describes accurately as a stiff¬ 
ness. He states that it is rather worse during the first few steps 
that he takes, particularly if he has been resting for a while; 
this, however, is certainly not pronounced, and I could not verify 
it objectively. He knows of no other circumstance, such as fatigue, 
time of day, etc., that in any way modified the symptom. 

Examination -■—The boy is intelligent and more advanced in 
his studies than is usual of boys in his station. His visceral 
organs are sound, and there are no indications of past syphilis. 
His cranial nerves, articulatory capacity, and sense organs are 
normal, as are his organic reflexes, and there are no sensory 
changes or defects in co-ordination. There are no trophic dis¬ 
turbances ; the feet are bluish, but not cold. 

Attitude .—Both feet are in a position of talipes equinovarus 
with pes cavus. This is much more pronounced on the right side. 
When standing he rests firmly on the left foot, but when doing 
so only the last two phalanges of the first two or three toes of the 
right side touch the ground; the right knee, and to a less extent 
the hip, is partly flexed and the thighs adducted. When he lies 
down the deformity is less, as it is also in a foot on which is 
placed the whole weight of the body; it can be made to disappear 
by passive manipulation. There is only very slight compensatory 
scoliosis, and no other deformity. 

1 The age and other points in the description are given as in January 1906. 



Motor System .—The development of the limbs is good, except 
that the legs are thinner than normal; the right calf measures 
21 centimetres at its maximum circumference, while the left 
measures 24. There is no local atrophy and no tremor of any 
kind. The lower limbs shew a slight diminution of power, but 
this would probably not have been called pathological had not 
other signs of disease been present ■, it is not confined to any 
particular group of muscles. Both lower limbs are markedly hyper¬ 
tonic, the right much more so than the left. The gait is obviously 
spastic, even approximating to a crossed-leg progression. The 
difficulty in walking is therefore made up mainly of two 
factors, the spasticity and the mechanical impediment due to 
the deformity of the feet and the contracture of the right lower 
extremity; it is only in slight part due to weakness. The 
muscular strength is very good elsewhere. 

Reflexes. — The knee-jerks and Achilles reflexes are very 
markedly increased. Ankle clonus, of the organic variety, and 
patellar clonus are easily elicited. When one strikes the tendons 
on the dorsum of the foot, flexion of the toes, especially of the 
three middle ones, follows, Bechterew’s sign being present. A 
crossed adductor-jerk is present. All these signs are more 
marked on the right side. The supinator and triceps-jerks are 
unduly active, as is the jaw-jerk, but the scapular-jerks were not 

Babinski’s extensor response occurs on both sides. The sign 
first described by Schafer, called in America Gordon’s paradoxical 
gastrocnemius phenomenon, is obtainable on both sides. Oppen- 
heim’s sign was not obtained, nor was White’s. The cremasteric 
and abdominal reflexes are normal. 

John, aged 17, is the eldest. Like all the other cases, he is 
not affected so severely as Ernest, and indeed is not prevented 
from earning his livelihood at various unskilled manual employ¬ 
ments. His gait is, however, so spastic that he can move along 
the street only at a slow pace; he uses no support. The talipes 
is just present on the left side, but is very decided on the right; 
the increase in the deep reflexes is more pronounced on the right 
side. The jaw-jerk was not obtained, but the supinator reflexes 
are very active. 

Arthur, aged 11, is affected to a considerably less degree than 
Ernest, and attends an ordinary elementary school in Mina Road. 


There is slight talipes on the right side, none on the left. The 
other signs resemble those of John’s, but the gait is decidedly 
better, so that he can join in the school games with fair 

Mabel, aged 9, is the only girl, and is the only child that has 
escaped. Her reflexes are absolutely normal, and there are no 
evidences at all of any nervous affection. 

The next two children, aged 7, are twins. Of these, 
William is affected decidedly more than Alfred. The result 
is that he, like Ernest, has to attend at the Centre for 
Physically Defective Children, while Alfred, like Arthur, goes 
to the ordinary school. William has talipes on both sides, but 
as it is not very advanced he can manage to hobble about 
pretty quickly, though not very securely. Babinski’s sign is 
present on both sides, but the ankle clonus, the increase 
in the deep reflexes, and the talipes are all more marked on 
the right. The supinator-jerks are active, and the jaw-jerk 
can be elicited. 

Alfred has only very slight deformity and spasticity. He 
can run about fairly well. The deep reflexes are obviously 
increased in the lower extremities, but not in the upper. 
Babinski’s sign and ankle clonus are present ; the jaw-jerk not 
so. The signs are all symmetrical. 

Henry, aged 5, is affected to a moderate degree. He can 
walk fairly well The supinator-jerks are active; the jaw-jerk 
was not obtained. The signs are symmetrical. 

Sydney, aged 3, shews the following signs equally on the 
two sides. The lower limbs are slightly spastic, and there is a 
commencing talipes. The knee-jerks are markedly increased, as 
are the adductor- and supinator-jerks. The jaw-jerk was not 
obtained. Patellar clonus is easily evoked, but not ankle clonus. 
The plantar reflex is usually extensor in type, but sometimes 
flexor. The boy can walk fairly well, though his feet scrape the 
ground at times. 

Albert, aged 1 A» is the youngest. He cannot walk or stand, 
but this is perhaps due to rickets, from which he suffers badly. 
It is difficult to estimate the tonus of the limbs, but they are 
certainly not rigid to any advanced degree. The knee-, supinator-, 
and adductor-jerks are all increased, and a crossed patellar reflex 
is easily obtained. A slight ankle clonus can be evoked. The 

• - •» . __ •*. 


plantar reflex is extensor in type. There is no obvious talipes. 
The signs are symmetrical. 

Summary of Cases. 

The cardinal signs are spasticity of the lower limbs, talipes 
cquinovarus, and changes in the reflexes indicative of an 
organic affection in the pyramidal tracts. It is a curious 
chance, and probably nothing more, that the signs are most 
marked on the right side in the four eldest patients, and sym¬ 
metrical in the four youngest. Paresis is only of the slightest 
intensity. The cardinal signs are present to an unequal degree 
in the different cases, and this is in no way proportional to the age 
of the patients. The spasticity and talipes can be correlated in 
degree fairly well; they are present in all but the youngest. 
The changes in the reflexes form indisputable evidence of an 
organic pyramidal lesion. The arm-jerks are increased in all the 
cases, but in none is there any other evidence of the upper 
extremities being affected. The jaw-jerk was obtained in only 
two of the cases, the two worst. In no case are there any 
pseudo-bulbar symptoms present 

Family History. 

For reasons indicated above, I think it worth while to give 
the family history in some detail, for one of the main obstacles 
to research on the types of heredity in such affections is due to 
the fact that writers so frequently content themselves with 
making negative statements. It is all-important to state pre¬ 
cisely not only how many individuals were affected, but how 
many were not affected. All the individuals mentioned below 
Are known positively not to have suffered from the affection, nor 
had any similar case been heard of by any member interrogated. 
The existence of the affection can therefore be excluded, with a 
fair probability, in the case of at least seventy members of the 
stock, including the members of the most important line for 
ever 150 years. 

Parents .—The parents are not related to each other. They 
Are healthy, and give no evidence, either in the history or by 


examination, of having had syphilis or any other relevant 
affection. They shew no abnormal physical signs in the 
nervous system. The mother has had no miscarriages, and none 
of her children have died. Her labours had progressed with 
moderate facility, instruments having been used in only two 
instances: even in these the children did not show any asphyxia 
or undue difficulty in starting respiration. 

Mother's Relatives .—The non-affection of the only girl in the 
childship naturally led one to suspect that the malady might 
have been transmitted through the females. I therefore paid 
special attention to the maternal line, and the female part of 
this in particular. Mrs Leach was the eldest child, and had one 
sister and five brothers in that order. The sister died at 30, 
leaving an only child, who is now an unmarried girl of 19. The 
brothers are all married, and all, except the youngest, have 

Mrs Leach’s father died of apoplexy at 41. Her mother 
was ninth in a childship of eleven. Of these, the eldest, a male, 
died of cancer of the lip. The second, a male, died of apoplexy. 
The next four were all unmarried females; only the last of 
these survives, aged 81. The seventh, a male, died late in life, 
cause unknown. The eighth, a woman, was married, but died 
without having any children. The tenth, a woman, had as 
offspring only one girl, who died of pulmonary tuberculosis 

without marrying. The youngest, a man of 69, is alive, 

and has extreme scoliosis dating from infancy. 

Mrs Leach’s maternal grandfather died at 65. He had 

one sister and three brothers. Her maternal grandmother died 
at 67. She had one brother and one sister; the latter had one 
child (male), who died in infancy. 

Father’s Relatives. — Mr Leach was eighth in a childship 
of nine. They all married and had children except the fifth 
and sixth, both sisters. His mother was the eldest child; 
she had two brothers. His father was also the eldest of six 

I append genealogical trees, so far as I could trace them. 
As regards the signs used therein, they are mostly those 
advocated by Mr Nettleship, and generally adopted. A wavy 
line = order of siblings 1 unknown. A bar indicates twins. 

1 Brothers and sisters ( QackwisUr) in the same childship. 



(?) = Number of siblings unknown. A circle = individual ex¬ 
amined by the writer. A square =» individual known to be 
dead. Present cases are indicated by dark shading. 




S S > 

*1. /* II 

\*Tl. William 

fiLPXto. Ha**y. snorter. ni.6t.HT. 
7. S 3 » 


0 — 07 ®—© 

© — S;® — © 





It is evident that we have to do with a diffuse affection of 
the pyramidal tracts, and, so far as the signs point, of them only. 
There is no indication of the presence of any local lesion. The 
three conditions chiefly to be considered are hereditary spastic 
paraplegia, transmitted syphilis, and Little’s disease. Of these, 
syphilis can certainly be excluded, for there we know of no 
form of the disease that will produce a progressive diffuse lesion 
of the pyramidal tracts at this age without giving rise to any 
other indication of its presence in either the parents or children. 
The freedom of the girl from disease is almost certainly more 
than a coincidence in a family of this size. As to Little’s 
disease, the facts that intelligence is unimpaired, that there 
is no strabismus, fits, or any other indication of intracranial 
affection, are all presumptive evidence against this diagnosis. 
There are, however, rarer cases of Little’s disease in which the 
effects of the cortical lesions are manifest only in the lower 
extremities. But it is most unlikely that this would happen 
in eight children out of nine in one family, and especially when 
there is none of the characteristic history indicating this cause. 
Further, the age at onset, and the peculiar mode of progress of 
the condition, in no way tallies with this supposition. 

In support of the diagnosis implied in the title to this paper, 
the following reasons may be adduced : affection of all the male 
children, the only female escaping; absence of any assignable 
cause; first evidences of the malady between the ages of one and 
two, this being so in all the cases ; striking similarity of all the 
cases to one another, the only differences being those of degree ; 
simila r course in all, namely, a very slowly progressive one, 
never reaching a condition of total incapacity; close resemblance 
in every detail to published cases which proved in fact to be 
transmissible through several generations. 

I use the word “ hereditary ” in preference to “ family,” 
because —granted the correctness of the diagnosis—the condition 
is hereditary in the scientific sense ; that is, it is due to an 
innate biological variation capable of transmission through a 
number of generations. In medical writings the word “ heredi¬ 
tary ” is often employed very loosely, for instance in the phrase 
“ hereditary syphilis ”; in this instance it is used to denote a 




condition that is not an inborn variation, and therefore not one 
transmissible through several generations. It might be prefer¬ 
able to employ the word “ family ” to describe such a condition, 
and others that may occur in different members of the same 
family, due to a common extrinsic cause usually infective in 
nature. It seems illogical to separate a class of case, such as 
that described in the present paper, from that in which cases 
are observed in another generation as well, calling the one 
" family ” and the other “ hereditary.” Such a distinction is 
practically meaningless, for it depends only on the extent to which 
the other generations are searched. Mr Nettleship has shewn 
clearly that the more extensive this search, the greater the 
number of cases that pass over from the family to the 
hereditary group, without of course there being any change 
whatever in the nature of the cases. That long intervals, even 
extending over several generations, may occur between the 
outcropping of such variations is of course in accord with what 
we know from biology of such variations. In the cases recorded 
in this paper, the original diagnosis would be only confirmed 
by the discovery, on the one hand, of additional cases in remote 
ancestors, or by the event, on the other hand, of similar cases 
occurring in the descendants—a fact that might be read as 
indicating that the present cases were the starting-point of the 
inborn variation in the stock. 





West Riding Asylum, Wakefield. 


The present investigation was primarily undertaken with the 
intention of demonstrating the changes in the achromatic struc¬ 
ture of the nerve-cells in pathological conditions. Two methods 
were principally used as representing two schools of teaching, 
viz. Bethe’s original and Lugaro’s colloidal silver method. The 
former shows the achromatin arranged as fibrils streaming 
through the cell, on the appearance of which the author has 
based his theories of nerve-cell relationship and conduction ; 
the latter shows the substance arranged as an interlacing mesh- 
work in the cells, and it is claimed by its author to be a much 
truer representation of the actual arrangement. It was found 
necessary to undertake an investigation into the arrangement of 
the structure in healthy states, and brain tissue from animals 
was used for the purpose. Other methods were also sometimes 
tried, viz. Ramon-y-Cajal’s No. 3 method, and the pyridin 
methods of Donaggio for the demonstration of the endo-'and 
pericellular structure. 

Intracellular Fibrillary Arrangement. 

In brief, Bethe originally claimed for the larger cells that a 
certain number of fibrils run through the apical process, cell 
body, and basal dendrites, a few pass from dendrite to dendrite; 
the fibrils are most numerous in the apical process, less numerous 
in the cell body, and fewest in the dendrites. The majority of 
the fibrils from the apical process form a reticulum round the 
nucleus—the deep or perinuclear reticulum. More superficially 
the fibrils are independent, and pursue a free course through 

1 Part of a thesis submitted for the degree of M.D. 



the cell. The axis-cylinder arises from the perinuclear reticulum, 
which becomes arranged into independent fibrils, much finer in 
calibre than those of the dendrites; it also contains a certain 
number of coarser dendritic fibrillse. 

The independence of the fibrils was criticised by Donaggio, 
who maintained that they form a network within the cell, denser 
round the nucleus, and showing more open- meshwork at the 
periphery. His conclusions in the main were supported by 
Rossi, Soukhanoff, Eamon-y-Cajal, Weiss, Azoulay, and Marin- 
esco. Towards the end of 1905, Donaggio published the 
results obtained by his pyridin and thionin methods. He 
alters his position somewhat, and describes two kinds of cells : 

(1) Those with endocellular network only; (2) those with 
endocellular reticulum and fibrils coursing through the cell, and 
maintaining their individuality. He declines to express an 
opinion with regard to the anastomosis of these long fibrils ; 
he believes the methods of Ramon-y-Cajal to be unsuitable for 
the demonstration of the very fine fibrils. He describes various 
condensations of the endocellular network, in addition to the 
perinuclear ring. With regard to the origin of the axis- 
cylinder, he describes four different positions in the cell from 
which it may arise : (1) From the periphery of the cell reticulum. 

(2) From the reticular thickening which is not perinuclear. 

(3) From the deeper portions of the cells and fibrils from the 
level of the nucleus. (4) Reticulum round the centre of the 

Rossi, Michote, and Lugaro believe there are no long fibrils ; 
the latter by his colloidal silver method says that there is anas¬ 
tomosis of the fibrillse throughout the cell, and also in the axis- 
cylinder, that lozenge-shaped spaces are thus formed which give 
the appearance of fibrillse when appressed. 

Founded on the results of his personal observations, Donaggio 
puts forward a theory regarding the function of the differently- 
constituted nerve-cells, viz.: in cells with endocellular network 
only, impulses are conducted only in one direction, and the re¬ 
ticulum is an apparatus for the reception and synthesis of stimuli 
transmitted by cellulipetal paths. In cells with two systems of 
fibrils, the long fibrils pass through the axis-cylinder, and might 
conduct impulses cellulifugally, whilst the reticulum within the 
cell receives the cellulipetal impulses. 



Personal Investigations. 

The material used was obtained from the ox, sheep, pig, and 
cat. The appearances presented by the cells from various parts 
differ considerably in the fibrillar and reticular arrangement. 
The ganglionic cells of the cortex have a much greater fibril lated 
structure than those of the medulla and cord. The arrangement 
seen in these cells differs very much from that met with in the 
smaller cells. By Bethe’s method the larger fibrils are distinctly 
shown, and in some cases there is a partial staining of the finer 
threads, but the general appearance is such as to confirm the 
opinion that the staining process is incomplete. The large 
Cells of the spinal cord do not show the apparently independent 
fibrils, but in their processes the appearances are similar to thoee 
met with in the cortical cells. 

The tissues prepared by the method of Lugaro show the 
achromatic structure arranged as an interlacing network, with no 
independent fibrils, and greater detail of structure is more clearly 
brought out. The results obtained by this method also vary, 
especially in specimens obtained from animals. The tissues 
were placed in the fixing agent immediately after the animal 
was killed; tissues from the human subject where the results 
were uniform were not obtained until a considerable period after 
death. The want of uniformity might be due to the action of 
the fixing agent on tissues before actual cell death had occurred. 

The small and large pyramidal cells present a simpler 
endocellular arrangement than the layer of giant cells. The 
anastomosing reticulum is more distinct, less elaborate, and the 
meshes are fewer in number. With regard to the appearance of 
the meshwork, the results obtained confirm those of Lugaro. 
The fibrillation seen in the apical process is only apparent, and is 
made up by the apposition of numerous diamond-shaped meshes 
of the reticulum; in the cell body they expand and become 
more open at the periphery of the cell, are smaller in the inter¬ 
mediate zone, and in the zone immediately round the nucleus 
they are smallest. 

At the origin of the axis-cylinder there appears to be no 
actual rearrangement of the structures within the cell. The 
endocellular network seems to be wholly prolonged into the axis- 
cylinder sheath and is consequently appressed; this causes a 



diminution in size of the reticular spaces at the cone of origin 
of the axis-cylinder. The cone itself is formed by the apposition 
of the meshes; this gives an appearance of a rearrangement 
having taken place, and also of long fibrils, especially at the 
periphery of the process. The cone may reach the perinuclear 
ring, especially in the human subject, where the endocellular 
network is more profuse and the axis-cylinder origin is conse¬ 
quently greater. In diseased states the connection with the 
perinuclear ring is the last to be destroyed. The dendrites can. 
be followed through the pericellular nets to the peripheral zone. 

The cells of the medulla and cord very much resemble each, 
other, the three-layered arrangement of the intracellular network 
being very distinct. Donaggio has described various condensa¬ 
tions of the endocellular network besides the perinuclear ring, 
but these condensations are very variable in their position and 
arrangement and might result from the sudden transition between 
the meshes of the different layers. The arrangement of the. 
fibrils in the processes is shown by Lugaro’s method to be a net¬ 
work. Bethe’s method fails to reveal the secondary fibrils 
which complete the network ; the interfibrillar substance is for 
the most part homogeneous. 

Applied to the cerebellar cells the method of Lugaro has not 
been successful. The wealth of connections of Purkinje’s cells 
is not seen; the basket arrangements round each cell are alsa 
very faintly indicated. This may be due to the latter structures 
being pericellular aud probably non-nervous. 

Pericellular Network. 

Three views are held with regard to its composition. It 
is—(1; a nervous structure; (2) neuroglial; (3) an artefact, 
Golgi and Martinotti first described it as neurokeratin, and the. 
latter looked upon it as an isolating body. Bethe found that 
his method stained it, and he believed the reticulum to be formed 
by the axis-cylinders of nerve cells and that it establishes con¬ 
tinuations with the neurofibrils of the cytoplasm. Ramon-y~ 
Cajal thinks it is not a real pericellular structure; Lugaro sup¬ 
ports this and thinks the appearances are due to the coarser 
meshes of the superficial layers of the spongioplasm. Marinesca 
thinks the appearances are artificial. Van Gehuchten thinks the 



presence of a network is doubtful, but it is not a conducting 
body. Perhaps the view advanced by Donaggio that the plexus 
is a demonstrable structure, that it is in close relationship to the 
nerve cells, but that it is of neuroglial origin and consequently 
has nothing to do with nerve cell function as that is usually 
understood, is the theory that finds most acceptance at the 
present time. In 1896 he described structures which he main* 
tained were similar to those described by Nissl, Ramon-y-Cajal, 
Semi Meyer, Aldren Turner, and Hunter, and which he believes 
to be neuroglial in origin. Further papers in 1904 and 1905 
serve to confirm him in his belief. Held, who formerly believed 
the structures to be nervous, now supports the view that they 
are neuroglial. In the meshes of the pericellular reticulum are 
minute ray-like structures which stain by Donaggio’s method and 
which are composed of a single centre which does not stain and 
numerous fibrils radiating out from it. “ Radiations ” or “ Rag- 
giere ” is the term given them by their author. Held confirms 
the presence of the radiations, and thinks they are the same 
structures described by him under the name “ Sternformigen 
Haufen ” ; he thinks they are non-nervous, but Donaggio does not 
give an opinion. Ramon-y-Cajal suggests that the central un¬ 
stained portions correspond to the “ Buttons of Auerbach,” which 
are impregnated by his method but are not coloured by 
Donaggio’s process. The embryological researches of Fragnito, 
Capobianco, Paladino, and Seniti support Donaggio’s view of the 
neuroglial origin. 

Do Nerve Cell Fibres Anastomose? 

Golgi thought that the axis-cylinder broke up into a network 
round the adjacent nerve cells ; Vassale and Donaggio suggested 
there might be an anastomosis between the geminulse on the 
protoplasmic prolongations of one cell and the axis-cylinder of 
another. In the cerebellum Hill thought it possible that the 
axis-cylinders of the granule cells ended in the gemmulse of the 
processes of Purkinje’s cells. Held believes in the continuity of 
the axis-cylinder and adjacent cell processes. In invertebrates 
Apathy, by means of his neurofibril method, demonstrated that 
primitive fibrils may run through several ganglion cells and form 
numerous anastomoses; he thinks the whole mass of nerve 



fibres is one continuous sheet of connections. Bethe supports 
Apathy’s views of anastomosis in the intercellular reticulum. 
Ramon-y-Cajal does not believe there is continuity, but considers 
that there is contiguity between the nerve cells and fibres, and 
that the chalices described by Held envelop but do not penetrate 
the cells. Veratti, however, regards these chalices as products 
of partial impregnation of a membrane which surrounds unipolar 
cells. By means of his newer processes, Ramon-y-Cajal has de¬ 
scribed structures on the cell body which he terms “ Buttons of 
Auerbach ” ; they are black, often granular, the centre is some¬ 
times clear, they are very numerous on the cell bodies and 
processes of the cells of the spinal cord and bulb ; they have not 
been demonstrated in the cells of the cerebral cortex. Van 
Gehuchten thinks that these buttons end independently on the 
cell body, that they do not form a network, and that they are 
the same as the structures described by Held and termed by 
him “ Endfusse.” The suggested relationship between these and 
the “ Radiations ” of Donaggio has already been mentioned. 

With regard to the nerve fibre terminations in the cells of 
the acoustic centre, it was thought by Held that the pericellular 
baskets which enveloped these cells were formed by adjacent 
nerve fibres, but in 1903 Donaggio was able to show that the 
axis - cylinders and the large nerve fibrils are distinct; he 
believes that the acoustic terminations of Held are not really 
nerve fibre terminations, but are part of a fibrillar conducting 

That specialised pericellular structures exist, must, I think, 
be allowed, at any rate in the larger cells of the cerebral cortex 
and in those of the medulla and cord. The colloidal silver 
method shows differentiated structures in each of these localities ; 
the cells show a reticulum, the meshes of which are more 
rounded and the fibrils are of finer calibre; it appears in con¬ 
tinuation with the cell body, is prolonged on to the dendrites and 
axis-cylinder, and is seen as a rudimentary web at the origin 
of the processes. The boundary of the cell is marked by a 
fairly regular line, on the outer side of which is the covering 
described. Further, the dendrites are sometimes seen passing 
out from the boundary of the cell and covered by a sheath, in 
the same way that the spinal nerves emerging from the cord 
carry a covering of the meninges. Adjacent cell processes can. 



be traced on to this net, but it is not determined whether there 
is actual fusing or not Regarding the nature of these struc¬ 
tures, they are probably different in constitution to the nerve- 
eells, and are probably of the nature of specialised neuroglia. 
In this connection the findings of Donaggio are of the highest 
importance, and point to an ultimate solution of the difficulty. 

Development of Nerve-Cells and Fibres. 

Before considering the functional activity of the nerve-cell, 
it is necessary to review the work that has been done of recent 
years on the development of the nerve-cell and its fibres. Up 
to recent years the theory that each nerve-cell and its fibres was 
developed from a single unit was generally accepted. During 
the past six years or so, Fragnito and others have been en¬ 
deavouring to disprove this. In the chick he shows the 
epithelial and the germinal cells to be quite distinct. The 
former form the neurospongium—a substance of great tenuity, 
which contains blood and lymph vessels. Neuroblasts appear 
later as deeply staining, round or oval bodies, which tend to 
form groups, and to wander away from the neural tube. Each 
group is composed of: (a) primary neuroblasts—may be one 
or more—which form the nucleus of the adult cell; (b) 
secondary neuroblasts—several in number—which form the 
various parts of the cell protoplasm. There is no karyokinesis. 
Later the secondary neuroblasts lose their contour, fuse together 
surrounding the primary neuroblasts, and so completing the 
appearance of the adult cell. Capobiauco confirms these find¬ 
ings ; he compares the number of nerve-cells formed with the 
number of neuroblasts, and he finds that in two cases the propor¬ 
tions were 1 to 2*83 and 1 to 3*02. These findings lend 
considerable support to the theory. 

In 1903 Fragnito also dealt with the development of the 
peripheral nerves, and sought to show that they were developed 
from rows of cells which gave rise to two processes. These 
processes unite with similar ones from other cells, so that a 
beaded fibril results—the beaded appearance being due to the 
persistence of the cell. By the coalescence of a number of fibrils 
a fibre is formed; the axis-cylinder and dendrites grow as 
distinct structures after this manner, and when complete, one 



end becomes fused with the secondary neuroblasts at the edge 
of the cell body. 

Of late years also much attention has been directed to 
regeneration of nerves after injury. The older theory of 
Wallerian degeneration and regeneration from the central end 
of the divided nerve has been severely criticised. The peripheral 
theory of regeneration was started by Btingner in 1891, and has 
since been strongly advocated by many writers. Degeneration 
begins in the peripheral end in a few hours, and is complete in 
three to four weeks. The nuclei of the neurolemma sheath 
take on the functions of neuroblasts, become arranged in rows, 
and in course of time give rise to axis-cylinder and myelin 
sheaths. Bethe claims to have demonstrated this experimentally, 
but his results were adversely criticised by Miinzer. Fleming 
thinks that both central and peripheral regeneration occurs. 
Cases of rapid reappearance of sensation (one to two days) after 
accident is attributed to nerve-twig anastomosis, or to peripheral 

Considerations on the Neuron Theory. 

Since the theory of the pluricellular origin of nerves has 
received so much attention of late years, the neuron theory 
which is built on the single cell theory has been vigorously 
attacked. Golgi never accepted the theory, and was the chief 
critic between 1891 and 1897. His criticisms were supported 
by Apathy’s researches on invertebrates, and Bethe’s work on 
vertebrates was similarly directed; the latter observer en¬ 
deavoured to show that nerve function took place in the inter¬ 
cellular network where the neurofibrils anastomosed ; he attempted 
to support his conclusions by experiments, but these were not 
conclusive. In 1898 and 1899 Lugaro attacked the critics, 
and foreshadowed a view which he later laid more stress upon, 
viz. that mere continuity of nerve-fibrils would not necessitate 
the destruction of the neuron theory; that were Bethe able 
to conclusively prove that acts took place in the intercellular 
network, and that the nerve-cells only exercised a trophic func¬ 
tion, it would not seriously interfere with the theory, in so far 
as it affirms an embryological and trophic autonomy. In in¬ 
vertebrates Lugaro suggests that a fibrillar anastomosis is com- 



petible with the performance of simple acts, but for finer nervous 
interworkings, as in the higher animals, it is more easy to 
establish associations in complex acts by simple contiguity. 
Van Gehuchten, Barker, and Ford Robertson support Lugaro’s 

Since 1900, Fragnito and others, basing their conclusions on 
the pluricellular origin of nerves, have added more criticisms 
against the theory. Durante, in the course of his criticisms, 
says that he believes that the fibres are not merely inert con¬ 
ductors, but that each segment takes part in the conduction of 
the impulse, and the relative slowness of nerve transmission is 
due to the time occupied between the neuroblasts, each of which 
is active in the process. In 1904 Bethe states the arguments 
for and against the theory, and remains unchanged in his posi¬ 
tion. About the same time Lugaro elaborates the views he 
expressed in 1899, and points out that the anatomical unity of 
the neuron is conceivable in two senses, viz. (a) in a narrower 
sense implying a cellular unity, (&) in a wider sense as an 
“ organic individuality,” as a complete organ, leaving unprejudiced 
the question of its embryological origin and of its cellular 
“ unity." 

In examining the evidence that has been brought forward 
against the neuron theory, it is seen that most of the criticism is 
founded upon results obtained by Bethe’s method. The author 
himself is the most zealous critic, but even he has been unable 
to demonstrate conclusively, either histologically or from experi¬ 
mental research, that there is a true anastomosis between the 
processes of one cell and those of another. The method itself is 
unreliable and inadequate to show the reticular arrangement. 
With regard to impregnation by silver nitrate, it is scarcely pos¬ 
sible to draw conclusions from the results. It would be better 
to continue to regard it only as a useful adjunct to anatomical 
study. The further elucidation of the relationships of the peri¬ 
cellular nets and “ radiations ” of Donaggio will probably help to 
throw further light on the mode of nerve-cell termination. It 
seems to me that the modifications which Lugaro suggests, viz. 
each cell as an “ organic individuality,” can scarcely be permitted 
if the neuron theory is to be maintained. Relationship by con¬ 
tiguity of cell to cell is the main argument for the theory ; and 
if continuity can be proved, it necessarily follows that nervous 



phenomena must be explained on a different conception of cell 
arrangement. Besides, it is not quite clear what Lugaro means 
by “organic individuality,” or how he proposes to correlate it 
with continuity of fibres. The embryological studies of Fragnito, 
Capobianco, and others, and the accumulating evidence of peri¬ 
pheral regeneration of nerve fibres, are certainly very suggestive ; 
but on a matter of such moment, and one so full of debate, there 
has been too little confirmation of the findings, and consequently 
it must still be held that the neuron theory is the best suited to 
explain the various nervous acts. 

Pathological Changes in the Neurofibrillar Elements of 


During the past six years various experimental researches 
have been carried out to demonstrate changes in the achromatic 
substance. These researches comprise results from four varieties 
of experiment, viz. cutting, evulsion, prolonged anaemia, and the 
toxins from tetanus and rabies. Three constant changes were 
noted, viz. (1) reaction, (2) degeneration, (3) reparation. The 
more severe the lesion, the more intense are the cell and fibre 
changes, but these changes are practically the same whatever be 
the lesion. The cells swell, then shrivel, nucleus is displaced, 
chromatolysis, loss of striation, powdery appearance of the chro¬ 
matic elements; the changes spread from the cell body to the 
fibres; the reticulum disappears. 

Marinesco has described regeneration of the achromatic 
structure after injury. The generated material differs from the 
original in that the strands are thicker, more opaque, and 

In various diseased states, e.g. myelitis, meningitis, and brain 
softenings, the changes have been described by Marinesco. 
Chromatolysis and breaking up of the fibrils go on side by side : 
they may commence either at the centre of the cell, at the peri¬ 
phery, or diffusely. 

The following notes are an epitome of an investigation into 
the changes met with in the achromatic substance of nerve-cells 
in about thirty cases of the insane. The specimens were routinely 
collected from the cases in the post-mortem room, and practically 
nothing was known about them until the microscopical examination 


was finished. The precentral convolution was always examined, 
in many cases also parts of the medulla, cord, and cerebellum. 

Group I .—Six cases. General Paralysis. Small pyramidal 
cells much reduced in number, and staining reaction-cell spaces 
frequently contain only traces of amorphous material. Large 
pyramidal layer—the cells are more distinct; fibrillation and 
pigmentation, especially at the base of cell, pronounced. The 
ganglion layer shows the cells much swollen and globose, or 
shrunken, their processes broken off; the pericellular net as a 
ragged covering; unequal staining of the cell body ; endocellular 
reticulum altered; the various condensations absent; the meshes 
huger, and their outline fainter. As is usual, much cell pigment 
is present, and is contained in meshes larger, more rounded, and 
coarser than those usual to the cell. Figs. 4, 5, 6, 8. 

Group II.—Organic Dementia , in which cerebral softening has 
occurred. The general character of the changes resemble those 
met with in the former group, but the cell disintegration is 
greater; the brain tissue was softer, peri- and endarteritis were 
pronounced—small pyramidal cells very fragmentary—the cell 
outline of the large pyramids was very faint; many large 
neuroglia-cells seen packed between the nerve-cells — axis- 
cylinders varicosed, thickened, and irregular—the nucleoli of 
the ganglion cell layer deeply stained, in contrast to the 
faintly-coloured nuclei and cytoplasm—pigment much increased 
—Purkinje’s cells faintly coloured—the cells of the medulla 
and cord are in a state of very advanced degeneration, so that 
almost no healthy structure was seen. The cell processes and 
endocellular network seemed almost completely destroyed. For 
some time before death the patients were bedridden and helpless. 
Figs. 7, 9, 10. 

Group III. — Dementia associated with various physical dis¬ 
orders—chronic interstitial nephritis—tuberculosis of kidneys 
and lungs. The intracellular structure of the small pyramids 
was not so disorganised as in the other cases; fibrillation per¬ 
sisted in the processes—the cells of the large pyramids were 
fairly numerous, but unevenly stained, the nuclei were usually 
displaced—the axis-cylinders were often well shown—pigment 
fairly large in amount—remains of perinuclear ring present— 
pericellular reticulum fairly well shown—interfibhllar spaces 
larger. Fig. 11. 



Group IV. —Contains a series of six cases of Chronic Brain 
Atrophy. Great diminution in size and number of small pyra- 
mids, and also much alteration in shape—large pyramids simi¬ 
larly affected—endocellular network indistinct, fragmented, and 
granular—ganglionic cells similarly affected, and contain much 
greenish coloured pigment. 

Group V. —Two cases of Epileptic Dementia. The structure 
of the small and large pyramidal cells is more profoundly 
affected than in any other condition examined—there is no 
trace of reticulum in the cells of either layer—the ganglionic 
cells are much altered. The medullar and nuclear are merely 
outlined. In the cerebellum the cells of the granule and 
molecular layers appear to be numerically less. 

Group VI. —Includes one case of Diabetes MeUitus associ¬ 
ated with Melancholia. The chief point of interest in this case 
is the want of staining of all the cells in the cortex, medulla, 
and cord, whilst those in the cerebellum were only faintly 
coloured. The intercellular substance was beautifully coloured, 
and by Lugaro’s method the sections had the appearance of 
Weigert - Pal preparations; the cell spaces were empty, or 
contained only a little debris. Fresh collargol and control 
sections which stained well were tried, but with a negative result. 
The patient had suffered from diabetes for a number of years, 
and died of diabetic coma. The pancreas was much diseased. 
Fig. 12. 

Group VII.—Chronic Mania associated with Tuberculosis 
and Fatty Heart —three cases. The percentage of stained cells 
in the small and large pyramidal layers is much larger than in 
other groups—the appearance suggests that the stage of disinte¬ 
gration is less advanced here. Although the ganglion cells 
present the usual features of disintegration, it was noted at 
the time of examination, and before the mental state was 
known, that the changes were not so advanced. In the 
cerebellum the intercellular substance of the granule layer is 

As a result of these observations it is seen that the achro¬ 
matic structure of the cells is profoundly affected in mental 
diseases, and that the changes differ chiefly in degree rather than 
in kind in the various conditions. The case of diabetes mellitus 
presents very unusual features, but as it is a single case, and so 



lacks confirmation, too much stress is not laid upon it, and it can 
only be regarded as an interesting condition. 

Much has been written about the significance of pigment in 
nerve-cells, as its presence is such a constant feature in diseased 
conditions. It is most frequently found at the part of the cell 
where there is supposed to be greatest functional activity, 
although this is not always so. It is contained in a reticulum 
which differs from that of the cell proper, in that the meshes are 
larger, more irregular, and the fibres which form the meshwork 
thicker. Marinesco thinks that the pigmentary reticulum is 
distinct from that of the cell, and the appearances presented by 
the specimens under examination go to confirm that view. The 
fact that it tends to increase in old age, and in the more chronic 
diseased mental states associated practically constantly with 
disease of the blood-vessels, implies a gradual interference with 
the normal nutritional supply to the tissues; and it is easily 
conceivable that such a reduction of nutrition would result in 
diminished metabolism within the cells, and so to an accumula¬ 
tion of partially reduced effete bodies which appear as yellow 


1. Mann, O. *“ Physiological Methods and Theory,” 1902. 

2. Lee, Bolles. “ The Microtomist’s Vade Mecum,” 1900. 

3. Schkfer. “ Text-book of Physiology,” 1900. 

4 Schafer. Essentials of Physiology,” 1900. 

5. Ford Robertson. “ Text-book on the Pathology of Mental Diseases,” 

6. Strieker. M New Sydenham Society,” voL i, 1870. 

7. Bianchi. “ Text-book of Psychiatry,” Macdonald, 1906, 

8. SoukhanofL | “ Sur le reaeau endocellulaire de Golgi dans lea 414ments 

nervenx de l’4corce cerebrale,” Nevraxe, voL iv. fasc. i, 1902. “ On the 

intercellular network of Golgi of the nervous elements of the spinal cord 
in the adult superior vertebrate,” Journ. of Meat. Path., voL v., 1903 (Epitome). 
“Contribution to the study of the endocellular network in the nervous 
elements of the spinal ganglia,” Nevraxe, voL vi p. 76 (EpitomeX 

8. Soukhanoff, with Grier and Gurewitch. “ A contribution to the study 
of the protoplasmic processes of nerve cells,” Ibid., voL vi, 1904 (Epitome). 

9. Wundt’s “ Physiological Psychology.” 

10. Wilson, S. A. K. “A note on Cajal’s new method for staining neuro- 
fibrillae,” Rev. Neurol, and Prych., April 1904 

11. Marinesco. “The role of centripetal and centrifugal stimuli with 
regard to the function and nutrition of the nerve cell,” Rev. Neurol., No. 13, 
1905. “ Researches upon the structure of the fibrillar part of the nerve cells 



in normal and pathological states,” Rev. Neurol , No. 9, 1904 (Epitome) 
"New researches upon the neurofibrils,” Ibid., No. 15, 1904 (Epitome) 
“ Lesions of the neurofibrils in certain pathological conditions,” Ibid., June 

12. Donaggio. “The action of pyridin upon the nervous tissues, and 
methods for the selective staining of the endocellular fibrillar reticulum and 
peripheral reticulum of the nerve cells of vertebrates,” Rev. Neur. and Ptych., 
September 1904 “The endocellular fibrillary reticulum and its relation 
with the fibrils of the axis-cylinders,” Ibid., February 1905. “ On the special 
fibrillar apparatus in the nerve-cell elements of certain centres of the acous¬ 
tic,” Riv. Speriment. di Fren., 1903 (Epitome). “ On the question of relation¬ 
ship between the paths of the intercellular conduction and the periphery of 
the nerve-cell,” Ibid., f. 4, 1903 (Epitome). 

Donaggio and Fragnito. “ Lesions of the endocellular fibrillary reticu¬ 
lum in the cells of the cord, following tearing out of the sciatic nerve and 
the corresponding posterior roots,” Riv. Speriment di Fren., June 1905 
(Epitome). <j 

13. Fragnito. “ Lo sviluppo della cellula nervosa nel medullo spinale di 
Polio,” Ann. di Nevral., 1902 (Epitome). “ The extracellular paths of nerve 
cell conduction,” Ibid., f. 4, 1904 (Epitome). “ The genesis of the proto¬ 
plasmic processes of nerve cells,” Ibid., Anno 22, f. 2 (Epitome). “ On the 
genesis of the central nerve fibres and their relation to the ganglion cells,* 
Ibid., fasc. 1 and 2, 1905 (Epitome). “ On the genesis of the central nerve 
fibres and their relationship to the ganglion cells,” Ibid. (Epitome). 

14 Lugaro. “ Sul significato delle modificazone pathologische della parte 
cromatica della cellule nervose,” Riv. Spen'ment. di Frenat., 1902 (Epitome). 
“ On the structure of the axis-cylinder,” December 1905. 

14. Lugaro. .“On the present position of the neuron theory,” Arch, di 
Anat. 9 di Embriol, vol. iiL f. 2, 1904 (Epitome). “ A method of colouring 
neurofibrils by means of colloidal silver,” Monit. Zoolog. Ital., N. 3, 1904 

16. Rossi. “ The auric reaction and internal structure of the nerve cells 
of the human spinal ganglia,” Nevraxe, vol. v., 1903 (Epitome). “The auric 
reaction and the internal structure of the nerve cells of the human spinal 
cord,” Ibid., p. 173 (Epitome). “ The minute structure of the nerve cells in 
man, ” Ibid., vol. iv., 1904 (Epitome). “The fine histology of the giant cells 
of the human cerebral cortex,” Ibid., voL vii., 1905 (Epitome). 

16. Bethe. “Zur Frage der autogenen Nervenregeneration,” Neurol. 
Centralbl., Jan. 16, 1903. “The neurone theory and its present position,” 
Deutsche mod. Wchntchr., Aug. 1904 (Epitome). 

17. Lenhoss^k. “ Ramon-y-Cajal’s new fibril method,” Neurol Centralbl., 
M. 3, 1904. 

18. Bielschowsky. “The silver impregnation of neurofibrils,” Neur. 
Centralbl., No. 6, 1903. “The non-myelinated nerve fibres in the foci of 
multiple sclerosis : an answer to Strahuber,” Ibid., 1904 (Epitome). 

19. Ford Robertson. “A method of producing a selective deposit of 
silver in blocks of tissue and of obtaining sections suitable for toning with 
gold, platinum, or other metals,” Rev. Nebr. and Ptych., July 1904 

20. Durante. “The impossibility of the neuron theory,” Rev. Neurol., 

Plate ti. 

Mi Tfy 

‘mJu , w - u/mjuW* A - ***** **• 

1^/L nW w^ <( =^«' w 

, JL/*..{< M 4 ,V U*£« 

•Jl £t r ^JL*Jitc a/u laMf*’ 

ySr*d» 'ii kl*et*+** 

tU. ‘ ie -ir fe*»~ 


Fig. 2. 

5 *, *» <** 'rT 

&stt/*+ttU (jDrftr 

r>^.6 1% J Ctti: - 

B. :'£-./• UMJbt ^ . 

. .i.«A*vW rb-r*k~ ^ 

Fig. 3. 

Fig. 4. 



Pig. 3. Medulla of pig—large cell shows anastomosing reticulum in processes ; 
three layers of cell condensation ; prominence of perinuclear network; 
appearance of independent fibrils which are really anastomosing network; 
larger meshes at origin of axis-cylinder. (Lugaro.) 

Pig. 4. Male G.P. group of three cells from large pyramidal layer, showing 
inequality of staining. (Bethe—toluidin blue.) 

Fig. 5. Female G.P. group of three cells from ganglion layer; globose form ; 
internal reticulum much altered in form. (Bethe.) 

Fig. 6. Group of cells from the ganglion layer, motor cortex of a male G.P.; 
extensive pigmentation is seen in all the cells ; endocellular reticulum is 
fairly represented. (Lugaro.) 

Fig. 7. Male—Organic dementia—groups of three cells from ganglion layer; 
they are much swollen, extensively pigmented, distorted ; internal re¬ 
ticulum faint and much altered. (Leitz, £ 0. I. Bethe.) 

Fig. 8. Female G.P. cell in an early stage of degeneration, surrounded closely 
by connective tissue cells. ? Phagocytes. (Bethe.) 

Fig. 9. Male—Organic dementia—cerebral softening—axis-cylinders show¬ 
ing variations in size and varicosity. (Bethe.) 

Fig. 10. Female—chronic mania—cerebral softening—extensive pigmenta¬ 
tion of ganglion cell, which is cut obliquely; fibres composed of re¬ 
ticulum. (Leitz, £ O. I. Lugaro.) 

Fig. 11. Male—dementia following delusional insanity. Tuberculous kidney. 
Both cells show well-stained internal reticulum. A shows pericellular 
network ; B shows a peculiar elongation and pigmentation at the base of 
the cell. (Leitz, £ 0. I. Lugaro.) 

Fig. 12. Male — diabetes mellitus — melancholia — low power drawing of 
portion of cortex, showing absence of cell staining. (Lugaro.) 






(Beitr&ge zur histologischen Localisation dor Grosahirnrinde. 

Ffinfte Mittheilnng.) K. Brodmann, Jottm. f. Psychol, u. 

Neurol., Bd. 6, 1906, S. 276. 

The paper under review is Brodmann’s fifth contribution to the 
architecture of the cerebral cortex. The investigation is based on 
the study of the cell arrangement alone. The aim of the present 
contribution has been to ascertain how far the cortical structural 
areas which exist in man can be recognised in the lower mammals, 
and secondly to contribute to the discussion of the homologies of 

Only a small proportion of the interesting facts brought to 
light in the present paper can be referred to in an abstract; the 
general results are similar to those made familiar to English 
readers by Campbell’s publications, but the original article must 
be consulted by those interested in study of the brain, especially 
with regard to the localisation of function in the cortex. 

Brodmann’s description of the lamination of the cortex differs 
from Campbell’s in that he recognises only six instead of seven 
layers. His layer (1) is the lamina zonalis, which is devoid of cells; 
{2) includes the plexiform and small pyramidal cell layers of 
Campbell; (3) the medium-sized and large pyramidal cells; 
(4) the internal granular or stellate layer; (5) the layer of 
ganglionic or deep pyramidal cells; and (6) the deep spindle- 
shaped or polymorphous cells. Even in regions where one or 
other of these layers has disappeared, or where two or more have 
fnsed together, or where they are apparently increased in number 
by subdivision, the six-layer type is always recognisable during 
some period in the course of development This deviation from 
die type arrangement in the adult condition is well illustrated 
by the two structural areas which have been mapped out by 
the author in representatives of practically all the mammalian 
classes. The area gigantopyramidalis (precentral type of Campbell) 
is distinguished by the great reduction or absence of the fourth 
layer, though it is well marked in it during foetal life; while the 



calcarine type (area striata of Elliot Smith, visuo-eensory of 
Campbell), which is distinguished by a doubling of the fourth layer 
and the appearance of gennaris layer (lamina granularis inter¬ 
media) between the subdivisions, making the cortex appear eight¬ 
layered, has the typical six-layer type in the sixth foetal month. 

Many of the cortical types are more difficult to recognise and 
less typical in some of the lower mammals ; for instance, in many 
of the lower orders the fourth layer is not divided up, i.e. there is- 
no gennaris layer in the homologue of the area striata. Homo¬ 
logous cortical fields may be consequently dissimilar in structure. 

Area striata .—The topography and relations of this area in 
man is almost identical with the distribution of Campbell’s visuo- 
sensory type of cortex. From his earlier investigations of the 
European brain, the author was unable to accept Elliot Smith’s- 
statement that in many brains (those of Egyptians and Sudanese 
were studied by E. S.) the area striata extends on the lateral 
surface of the hemisphere almost up to the sulcus simialis (S. 
lunatus of E. S.—the homologue of the Affenspalte). But on 
examining Javanese brains it was found that Elliot Smith’s obser¬ 
vations on the Egyptian’s held here too, that the area striata 
extends on the lateral surface almost as far as the S. simialis, so> 
that from the similarity to the condition found in the higher apes 
it must be admitted that this fissure is the homologue of the 

In the higher apes (Orang) the extent of cortex occupied by 
the area striata on the mesial and lateral surfaces of the occipital 
lobe is about equal. The dorsal and ventral borders of the area 
striata are not limited on the lateral surface by the S. simialis and 
S. temporo-occipitalis lateralis, as has been asserted (Schlapp); in 
none of the apes does the area extend as far as the furrows, but 
the space by which it falls short of them is variable in different 
species. In the orang the area striata occupies practically the 
whole cuneus. 

In the lower apes the area striata is relatively much laiger than 
in man, and the greater portion of it lies in the lateral surface of 
the hemisphere. Whilst in man, too, the area extends to the sur¬ 
face of the gyri for almost the whole length of the calcarine fissure,, 
in the lower apes it lies buried for a considerable length of the 
oral part of the fissure, in many species the whole distance oral to 
the junction of its branches (involution, E. Smith), so that on the 
surface it is visible only in the caudal ends of the cuneus and 
lingual gyrus. There is not, however, “ complete involution ” of 
the area striata on the mesial surface of the occipital lobe in any 
of the apes, so Elliot Smith is incorrect in regarding the S. cal- 
carinus proprius of men alone as the homologue of the calcarine 
fissure of the apes, and in refusing to admit an homology between 



the human cuneus and that of the monkey, on the ground that part 
of the former is striate and the whole of the latter non-striate. 

In the lemur class the distribution of the area striata on the 
lateral surface is practically identical with that in the lower apes, 
but on the mesial surface it occupies the greater part of the cuneus 
and the posterior end of the lingual lobe, in this respect more 
closely resembling the anthropoid apes and man. Unlike the 
arrangement in the primates, the oral eud of the area is not buried 
in the calcarine fissure, but extends on to the surface of the lingual 

In the cheiroptera the area striata loses the topographical rela¬ 
tions to the sulci of the occipital lobe which have been described 
in the higher orders. Owing to the great development of the 
rhinencephalon, it comes to lie on the dorsal margin of the posterior 
portion of the hemisphere. 

The anatomical distribution of the area striata in the carnivora 
is of special interest, as Munk and Berger have localised the visual 
centre by experiment in the dog and cat in the dorso-caudal part of 
the lateral surface of the brain. B. has already pointed out that 
the centres outlined by these physiologists do not correspond to 
the area striata as determined by histological structure, and in 
this he is in full agreement with Campbell. The area striata 
occupies the caudal two-thirds of the lateral and medial surfaces 
of the gyrus marginalis. On the median surface the S. post- and 
supra-splenialis lie within it, and are probably the homologues of 
the S. retro-calcarinus (E. Smith). The area striata is bounded in 
part at least by the S. lateralis and splenialis; it does not at all 
correspond to Munk’s visual centre, and the latter does not coincide 
with any structural area. 

In the rodents and insectivora the area striata lies on the 
dorso-caudal surface of the hemisphere; it is more extensive 
laterally than mesially. There is no fissure which can be regarded 
as the homologue of the calcarine. In these orders the cortical 
structure is peculiar; it is relatively very broad owing to the great 
development of layers v. and vi., but layers ii. and iv. are very 

Koppen and Lowenstein have described the gyrus splenialis as 
the homologue of the area striata in Ungulates. B. has been 
unable to find any cortex of the area striata type in these adult 
animals, but he easily recognised it in foetal and new-born animals. 
In these it is easy to see that it occupies the same position as in 
the carnivora, i.e. in the gyrus marginalis, between the S. splenialis 
and S. lateralis, but it crosses the latter. 

Finally, in the marsupials the area striata occupies much the 
same position as in the lower apes, being situated on the dorso- 
caudal margin of the hemisphere, and more extensive on its lateral 



than its median surface. It is also distinguished by its histological 
structure being very similar to that of the primates, the fourth 
layer being divided up into three substrata, and by its relatively 
great extent and its sharp limits. 

It has been much more difficult to trace the area gigantopyra- 
midalis (the precentral area of Campbell) through the various 
orders of mammals, as it is often bounded by transition types, and 
in some species (the lissencephalic apes) two areas overlap. In 
the higher apes it extends further oralwards, especially into the 
upper two frontal convolutions, than in man, so that the size of 
the area relative to the surface area of the frontal lobes is greater 
than in man. In mau it extends to the bottom of the S. Rolandi, 
but in many of the apes not so deep in the wall of the sulcus, so 
that in even closely allied species the G. centrales may not be pure 
homologous fields. Also, in the lemurs, for instance, it extenda 
behind the sulcus which has generally been regarded as the homo- 
logue of the S. Rolandi, while in neighbouring species its caudal 
limit does not reach the sulcus. 

As neither the S. cruciatus or S. coronalis of the carnivora 
have the same topographical relation to the area gigantopyramid- 
alis as the S. Rolandi to this area in man, neither can be regarded 
as the homologue of the central sulcus. In the majority of the 
carnivora, in fact, the area gigantopyramidalis lies only behind the 
S. cruciatus, and in the cat it extends into both the G. sigmoider 
anterior and posterior. The S. coronalis never marks its caudal 
limit, as Koppen and Lowenstein have maintained. 

In the ungulates, in contrast to the carnivora, the greater part 
of the area gigantopyramidalis lies in front of the S. cruciatus. 

In the rodents and insectivora the position of the area resembles 
that in the lower monkeys, but a well-marked fourth layer, which is 
absent from the typical precentral cortex, extends into the area 
occupied by large (? Betz) cells. This also occurs in the marsupials, 
in which the area is relatively very small. 

The following statements selected from the general conclusions 
which end the paper are of interest. Of the different layers of the 
cortex the greatest variability is found in iv.; the greatest amount of 
histological differentiation in iii. and v.; and the greatest variation 
in breadth in vi. Ascending the mammalian series, iii. increases 
in size, while vi. on the whole diminishes. The degree of develop¬ 
ment of any cortical area may not be constant in any stage of 
evolution ; the same area may be more similar in animals of 
distant orders than in allied species. The area gigantopyramidalis 
and striata are most highly developed in the primates. 

The sulci are of much less value in the topographical localisa¬ 
tion in the cortex than they have been assumed to be. They may 
simplify surface localisation, but do not necessarily establish the- 



limits or positions of cortical structural fields. In many cases the 
sulci of different classes which have been regarded as homologues 
owing to their position or course are not homologues. 

The value of the work is increased by clarity of description and 
illustration. Gordon Holmes. 

(49) Meat. Path., YoL viii, No. 1, p. 1. 

The author has examined this tract in the medulla of an idiot 
with agenesia of the ocular globes and atrophy of some of the 
olfactory tracts. 

At the level of the pyramidal decussation there was found an 
area of triangular shape at the periphery of the lateral columns, 
with complete degeneration of the fibres. Within and behind this 
was a circular rarefied zone separated from the central grey matter 
by a thin band of normal fibres. At the beginning of the decussa¬ 
tion of the sensory tracts the position of these two zones changed, 
the triangular area lying external to the external end of the 
accessory median olive, with the rarefied zone immediately behind 
it At the level of the complete decussation of the sensory tracts 
the triangular degenerated area became circular in shape, and then 
semi-circular, embracing the lower end of the inferior olive, while 
the posterior degenerated zone was pressed backward against the 
ascending root of the fifth nerve. 

Helweg’s tract, therefore, in its upper part, has the shape of a 
groove (appearing in horizontal sections as a semi-circle embracing 
the external part of the bulbar olive). The fibres gradually dis¬ 
appeared opposite the lower two-thirds of the bulbar olive, and pro¬ 
bably ended in relation with the cells of its dorsal leaflet. From 
its topography the author would term this tract the Fasciculus 
Circumolivarius. J. H. Harvey Pirie. 


A. R. Allen, Joum. of Nerv. and Meat. Dis., Dec. 1906, p. 771. 

By this stain the writer has demonstrated that the posterior 
median septum and some of the lateral septa contain connective 
tissue continuous with the pia, and are not exclusively neuroglial. 
The steps of the method are as follows:— 

1. Harden material as for the Nisei method. 

2. Sections are placed in aqueous solution of azure II., 



steamed for two to three minutes, and allowed to cool for 
fifteen minutes. 

3. Wash in distilled water. 

4. Absolute alcohol until clouds of blue cease to be given off. 

5. Place in 20% phenol or toluol (boiling-point 110*-112°) for 

about one minute. 

6. Place in solution of eosin (Grubler w.g.) in absolute alcohol 

(alcohol 60, eosin 0*02-0*05), and as soon as the change 
from dark blue to purple becomes pronounced (from 5-60 
seconds) remove at once and 

7. Place in 25% carbol-xylol for differentiation. Remove 

before it turns pink. 

8. Pure xylol. 

9. Mount in balsam in xylol. 

The pia is stained a vivid pink, and the sub-pial neuroglia tissue 
blue. The nerve cells are well stained also, and there is a differ¬ 
entiation in the walls of the blood-vessels, the intima and media 
staining blue, the adventitia pink. 

With material hardened first in formalin, then in Muller’s 
fluid, the Nissl granules are preserved and the axis-cylinder pro¬ 
cesses are stained blue, but the differentiation between the pia and 
the sub-pial neuroglial tissue is lost. J. H. Harvey Pirie. 


SPHERE. G. Mingazzini and O. Polimanti, Journ. of Mod. 
Path., Vol. viii., No. 1, p. 14. 

The authors have performed homolateral and contralateral hemi- 
fronto-cerebellar extirpation in dogs; cerebellar removal followed 
by frontal, and vice versa. They find that homolateral extirpation 
is followed by ataxia and asthenia on both sides of the body, but 
more marked on the side of the extirpation—very similar, in fact, 
to bilateral cerebellar removal. Contralateral extirpation produces 
only one-sided effects—that on which the cerebellum is removed— 
but the disturbances are far more marked than those following 
isolated hemi-frontal or hemi-cerebellar extirpation. The conclu¬ 
sion seems to be that each frontal lobe has an indirect action on 
co-ordinate movements of the limbs on the opposite side, and par¬ 
ticularly on the anterior limb. J. H. Harvey Pirie. 





(52) OF NERVES AFTER THEIR SECTION. (Prfcocittf des 
Fhfoomdnes de R6g6n6reccence des Nerfs aprbs lour section.) 

Marinesco et Minea, Comptes rendue des stances de la Soc, de 
Biol., T. bri., p. 383. 

This is a short note dealing with the phenomena of regenera¬ 
tion found twenty-four hours after section of a nerve. Some of 
the axis-cylinders swell and dissociate longitudinally into fascicles 
of neurofibrilke; these interlace with each other and with those of 
neighbouring axis-cylinders, and may in their turn divide, giving 
rise to secondary branches, some of which end in a cone of 

Another equally early mode of multiplication is by collateral 
division—fine fibres become detached from the axis-cylinders, 
constituting the first stage of the spiral apparatus previously 
described by the authors and by CajaL 

Multiplication by formation of terminal arborisations also 
occurs at this early stage. In all modes a close relationship is 
found between the young axones and the “ apotrophic ” cells. 

J. H. Harvey Pirie. 



(53) SPECIFIC FEVERS. Sir Thomas Barlow, Brain, 1906, 
p. 303. 

.Sir Thomas Barlow was singularly happy in his choice of a 
subject for his presidential address to the Neurological Society of 
the United Kingdom. In the consideration of this wide and 
fascinating subject the president brings out in striking manner the 
importance of the recognition of these complications to the general 
physician as well as to the neurologist. Many of the cases which 
he uses as illustrating some of the complications of the specific 
fevers are taken from his own experience, and similar cases are 
cited from the literature. By correlating the clinical side with the 
morbid histology, he not only throws direct light on many points, 
but makes valuable suggestions for the future investigation of 
many problems as yet unsolved. It is impossible to single out 
special portions for notice, as the whole address is devoted to a 
broad and general survey of a field of medicine which as yet has 
not received the attention it demands and merits. 

T. Grainger Stewart. 




(54) (L’Alcool e le malattie del aistema nervosa.) L. Bianchi, II 
Tommasi, Giomale di Biologia e Medicina,, Anno 1, N. 23, 1906. 

This is a lecture introductory to the author’s clinical course upon 
nervous and mental diseases. The known facts regarding the 
toxic action of alcohol, the changes the substance undergoes within 
the body, and its action upon the mental functions, and statistical 
evidence from various countries bearing upon the relation of 
alcoholism to disease and crime are first summarised. The 
author himself assigns to alcoholism in the parents a very 
potent influence in the causation of idiocy, imbecility, and other 
less pronounced forms of intellectual defect, as well as of epilepsy, 
severe hysteria, criminality, etc., in the descendants. In this 
connection he mentions that he has observed two families, all the 
members of which suffered from Friedreich’s ataxia (which he 
looks upon as dependent upon imperfect development of the spinal 
cord, a variety of spinal or spino-cerebellar idiocy corresponding 
to defective development of the frontal lobes, or the speech areas, 
in some microcephalic idiots), and the sole cause to which the 
morbid condition could be attributed was great abuse of wine by 
the parents. Although alcoholism is less prevalent in the south 
of Italy than in the north, its percentage incidence in the latter is 
nevertheless very high, and even alarming. Out of 1814 patients 
admitted to the asylum at Naples from 1901 to 1905, there were 
314 whom Bianchi definitely ascertained to be alcoholics. The 
author also touches upon the probable causes of the special 
tendency to the abuse of alcoholic drinks manifested by industrial 
workers. He thinks that there is perhaps an unconscious effort 
to make up for deficiency of food by taking alcoholic beverages, 
or to counteract the mental depression that is produced by the 
existing intellectual, physical, and social conditions. In the south 
of Italy, where there are practically no industries, the distribution 
of alcoholism coincides closely with the malarial zones, and this 
fact is probably dependent upon the mental and bodily depression 
induced by malarial infection and deficiency of food. Although 
acute alcoholic intoxication is very rare in southern Italy, drunk¬ 
enness from wine is extremely common, and Bianchi considers it is 
probable that much, not only of the epilepsy, crime, and idiocy 
that occur in this region, but also of the corpulence, indolence, 
indifference, rarity of noble impulse, excitability, irascibility and 
impulsiveness displayed by the population may be due to exces¬ 
sive use of wine. With regard to remedial measures, Bianchi 
expects more from education than from legislation, and in this 
process of education of the people he maintains that the doctor 
must take a leading part. W. Ford Robertson. 



(55) MYASTHENIA GRAVIS. (Contribute clinico alia conoscenza 
del morbo di Erb-Goldflam.) E. Levi, Bivist. di patol. nerv. e 
meni.y 1906, pp. 404 and 441. 

This is an elaborate and detailed account of nine cases of 
myasthenia gravis observed by the writer. He analyses the symp¬ 
tomatology of each case with minute care, but no new facts of 
interest are brought out. He considers the characteristic features 
of the disease to consist in the intermixture of bulbar symptoms 
with an external ophthalmoplegia, generally incomplete, and with 
a peculiar weakness and easy exhaustion of the musculature of the 
trunk and limbs, usually slow in onset but developing step by 
step, muscular asthenia always overshadowing paralytic phe¬ 
nomena. Certain muscular groups are attacked by preference; 
the disease is a remittent one, the myasthenic reaction is frequently 
present, and at the acme of the disease there may even be a degree 
of muscular atrophy. 

Most cases begin with ocular symptoms, in the form of uni¬ 
lateral or bilateral ptosis or diplopia. And whatever symptom be 
the initial one of the disease, that one generally remains the most 
persistent phenomenon throughout the course of the malady. 

The author is somewhat confused in his description of the 
myasthenic facies. He mis-quotes Gowers’ description of the 
“ myasthenic smile,” and is of opinion that it resembles that of 
facial myopathy, whereas Gowers clearly points out the difference 
between the facies in the two diseases. Levi emphasises the 
occasional presence of slight muscular atrophy in severe cases of 
myasthenia, so that this feature cannot be regarded as an absolutely 
differential point in the diagnosis from progressive muscular 
atrophy. The myasthenic reaction to faradism is by no means a 
constant phenomenon; it may be absent throughout the entire 
course of the disease, though this is unusual. The prognosis of 
the disease, according to Levi, is not so immediately grave as some 
authors would have us believe. The malady may remain quiescent 
for sixteen or more years before proceeding to a fatal termination, 
though this duration is the exception. As to treatment, the main 
object is the avoidance of fatigue, physical or mental; if diffi¬ 
culty of deglutition appears, special feeding with liquids or seini- 
solids must be resorted to. Feeding with the stomach-tube is not 
recommended, because of the liability to produce inhalation pneu¬ 
monia. Pregnancy is always to be feared, and may be the direct 
cause of death. Oppenheim has called attention to the frequency 
of congenital malformations in myasthenic patients; thus, for 
example, bifid uvula, unilateral congenital ptosis, polydactyly. 



webbing of the toes, micrognathy, etc., have all been described. 
The various pathological appearances in the muscles and lymphoid 
tissues are referred to, and the writer is of opinion that, notwith¬ 
standing the absence of positive pathological appearances in the 
central nervous system, it is incredible that there is not some 
obscure change in the nerve elements themselves. A copious 
bibliography completes a somewhat diffuse paper. 

Purves Stewart. 

M7ATONIA CONGENITA. [Zur Kenntnis der sogen. angeborenen 
(56) Muskelschlaffheit, Muskelschw&che (Myohypotonia, Myatonia 
congenita).] Bernhardt, Neurol. Centralbl., Jan. 2, 1907, p. 2. 

The condition under consideration is a very obscure one and the 
literature is scanty. It is not always quite easy to understand the 
exact point of Bernhardt’s somewhat lengthy argument, but as far 
as the abstractor can follow him, his main contention is that 
myatonia is due to degenerative or neuritic changes in the 
peripheral nerves, as opposed to Oppenheim’s view that the disease 
is a delay in the development of the muscles. Bernhardt recalls a 
paper written by him in 1904, in which he pointed out that in 
certain lesions of the nervous system, groups of muscles which 
were not, and never had been, paralysed, might give the reaction of 
degeneration. He at the same time described two cases of children 
in which this state of matter existed; in one case the legs only, in 
the other the limbs and neck muscles, were paralysed, while all the 
muscles, including those which could be moved, gave the reaction 
of degeneration. These cases (which ultimately recovered) he 
regarded as polyneuritic, and from the peculiarity of the electrical 
reactions thought that “ it [i>. the degenerative or inflammatory 
process in the peripheral nerves] would probably be one of those 
forms which, in addition to showing the changes in the peripheral 
nerves that lead to Wallerian degeneration, also show that form of 
neuritis described by Gombaultas the pre-Wallerian, in which there 
is a lesion only of the medullary sheaths.” In myatonia it seems 
more likely that there is delayed development of the peripheral 
nerves than delayed development of the muscles. Bernhardt 
next refers to Oppenheim’s view that there is a congenital defect 
of the muscles, and then mentions the findings at the autopsy on 
fcjpiller’s patient. In that case lesion of the thymus was present, 
and Bernhardt suggests that there may be some connection 
between this and the disease in question, taking as an analogy 
the delayed involution of the thymus sometimes met with in 
myasthenia gravis. The writer next discusses the question of poly¬ 
neuritis in early infancy, holding that it is not so rare as has been 



thought, and hinting (for example) that some of the reported 
instances of poliomyelitis acuta followed by complete, or almost 
complete recovery, were really polyneuritic in their nature. In 
most of the reported cases of myatonia, he states, the electrical 
reactions are diminished or absent. It is a strong point in favour 
of the disease being due to nerve lesion that, as in Gombault’s 
“periaxile neuritis,” non-paralysed muscles exhibit the same reactions 
as the paralysed ones do. The following additional points may be 
noted: In Bernhardt’s cases the lower limbs were most affected. 
The disease occurs only in early life, but whether it is ever 
actually congenital is doubtful. J. S. Fowler. 

(57) PLEXUS. W. B. Warrington and Robert Jones, Lancet, 
Dec. 16, p. 1644. 

This paper is based on the study of 30 cases, their treatment re¬ 
sulting in 11 recoveries—18 were cases of injury (falls on shoulder, 
etc.), 1 case, which was a dislocation of the shoulder, ending in 
recovery ; 8 were obstetrical in origin, and 4 resulted from neuritis. 

In regard to the pathology of the lesion, the authors assert that 
their cases lend support to Clark, Prout, and Taylor in their con¬ 
tention that the laceration, tearing or tension of the nerve tissues 
is commoner than simple pressure by bone or inflammatory 
material. Some of the signs of loss of nerve function exhibited 
by these cases shed light on the anatomy and physiology of the 
brachial plexus; they also have an important bearing on the prog¬ 
nosis of these palsies. 

Two cases are mentioned illustrating the absence of sensory 
defects in lesions of the upper root of the plexus. In one case 
paralysis of the muscles supplied by the fifth root, without any 
anaesthesia, resulted from the division of a nerve root during the 
removal of a large tumour from the neck. 

In the other case, exhibiting paralysis, but no sensory defect, 
during an operation for secondary suture the nerve trunk was 
divided at the junction of the fifth and sixth roots for the purpose 
of anastomosis with seventh root: as a result there was no further 
palsy, but an area of anaesthesia appeared over the deltoid area and 
over the outer half of hand and lower forearm. 

The authors think that Harris’s suggestion, in regard to the 
path taken by the motor fibres of the circumflex and musculo¬ 
cutaneous nerves via the fifth root, and by the sensory fibres of 
these nerves via the sixth root, is borne out by these two cases. 

These two cases also support Harris’s view of the extent of the 
motor supply of the fifth root (prefixed type) embracing, in addir 



tion to the deltoid and forearm flexors, the radial extensors and 
the pronator radii teres. The assistance afforded by the nature 
and extent of the anaesthesia in the diagnosis of the site of lesion 
is illustrated by a case in which the muscular palsy and the pupil 
changes indicated the 8th C. and 1st D. roots as the site of the 
lesion: the sensory changes, being of the dissociation type, con¬ 
firmed the radicular origin of the lesion. A case where the 
anaesthesia was similar in distribution, but not of the dissociation 
type, was mentioned by way of contrast; here a lesion of the 
ulnar and int.-cutaneous nerves was diagnosed and confirmed. 

The authors have studied the behaviour of the paralysed 
muscles under electrical stimulation, and have been impressed by 
the complexity of the question and the frequent difficulty of 
giving a correct prognosis. 

Two of their cases, in which the affected muscles gave the 
complete R.D. (Head and Sherren type), showed no sign of 
recovery in several years; on the other hand, a case exhibiting 
incomplete R.D. only gives no indication of recovery after seven 

Having mentioned the important bearing of the site of lesion 
upon prognosis, the authors enumerate some anatomical facts of 
interest. For convenience of description the spinal roots are 
divided into intra-, inter-, and extra-vertebral parts. 

The following clinical guides to lesions of these parts are 
mentioned: (1) pupillary changes result from in ter-vertebral 
lesions; (2) palsy of rhomboids, serratus magnus, and levator 
anguli scapulae denote a lesion proximal to extra-vertebral portion ; 
{3) paralysis of spinati denotes a lesion proximal to the junction 
of fifth and sixth roots : this is a more constant and reliable guide 
than 2. 

The authors state that the gravity of the prognosis increases 
with proximity of the lesion to spinal cord, and diminishes with 
accessibility of the lesion to surgical interference. The situation 
of the lesion is stated to be most commonly radicular. 

In regard to treatment, the importance of mechanical appli¬ 
ances in combination with massage, prior to operation, is insisted 

The signs due to loss of nerve function give no indication of 
the nature of the lesion, whether due to simple pressure upon, or 
to severe laceration of, nerve tissue. In the latter event, operation 
would be imperative; whereas in the former case, spontaneous 
recovery may ensue. Since signs of spontaneous recovery will be 
manifest within seven months, the authors think that mechanical 
treatment should be persevered in for at least this length of 
time, and the withholding of such measures is, in their opinion, 



The appliances utilised are a light malleable metal splint 
for the wrist and a sling: by means of the splint, the wrist can be 
maintained in the hyper-extended position and the extensor 
muscles relaxed, and by means of the sling the elbow is kept 
acutely flexed and the flexors of the forearm relaxed. 

This postural shortening of the paralysed muscles in combina¬ 
tion with energetic massage places them under the best conditions 
for recovery; the bandages fixing the splint should overlie tendons 
only and never the muscle belly. 

These methods failing after at least seven months’ application, 
surgical interference should be undertaken if the signs denote 
accessibility of the lesion. 

The authors discuss the various methods of operating for 
secondary nerve suture—end-to-end junction, anastomosis, nerve 
transplantation, eta; the former method they regard as ideal, but 
not always available in brachial plexus lesions. They draw atten¬ 
tion to the fact that part only of the nerve trunk may be involved, 
and that careful electrical testing of bundles may avoid unneces¬ 
sary division of nerve fibres : rigid asepsis on the part of assistants 
applying these tests is insisted upon. 

When adhesions are feared, after extensive dissection in fibrous 
tissues, the nerve ends may be surrounded by sterile foil. 

After healing of the operation wound, the postural shortening 
of lengthened muscles, with massage, should be practised. 

Several cases are related where this line of treatment met with 

The authors arrive at the following conclusions as to prognosis 
unmodified by surgical treatment:— 

1. “ That the condition is a serious one, only from 30 to 40 
per cent terminating in useful recovery. That birth palsy of any 
severity less commonly results in good recovery than the corres¬ 
ponding condition in adults. That the cases due to a local neuritis 
are a good deal more favourable than when injury is the cause.” 

2. “ That the lesion is commonly severe (laceration, eta) rather 
than due to simple pressure.” 

3. “ That a complete block of conduction with a corresponding 
graver prognosis may be diagnosed from (a) a consideration of the 
extent and kind of anaesthesia (Head and Sherren); ( b ) a study of 
the electrical reactions, especially with the constant current, but 
that the presence of full R.D. is compatible with complete 
recovery; and (e) attention to the extent and distribution of 
muscular palsy. 

“ The order of gravity of prognosis is lesions of the spinal cord, 
roots, plexus proper, peripheral nerves.” 

4 “ That if spontaneous recovery happens, some signs of it are 
visible within seven months in adult palsy, but that in birth palsy 



signs of recovery may be delayed for a longer period but are com¬ 
plete within a year. In birth palsies partial recovery is frequent, 
leaving the residual paralysis to be treated surgically.” 

Author’s Abstract. 

(58) PAU3IE8. (Die SensibilitfttsstSrungen bei peripheren 
GesichtaUthmungen.) Donath, Neurolog. Centralbl., Nov. 16, 
1906, p. 1039. 

Both subjective and objective alterations in sensation over the 
face affected by peripheral palsy have often been noted. In 58 
cases of facial paralysis, Scheiber noted 26 in which there was 
hypftsthesia to touch, pain, and temperature, which concerned 
the whole of the affected area, more rarely a portion of it, and 
still more rarely the mucous membrane of the tongue and mouth. 
Many other, rather differing, results might be cited. Donath has 
for Borne years carefully examined all the cases of this condition 
coming under his observation, paying attention, not merely to the 
face, but to the whole of the body, with the following result: 
in 43 facial palsies, facial sensibility was diminished 20 times, 
unaltered 25 times, increased twice; over the whole of the 
corresponding half of the body it was diminished in 15 cases, 
unaltered in 26, and increased in 2. Thus, only in 5 cases (11*5 
per cent.) was the diminution in sensation confined to the affected 
face alone. In 175 cases of peripheral facial palsy which he ob¬ 
served, 75 (42-9 per cent.) suffered from subjective pains over 
the affected area or over neighbouring areas. They varied in 
duration from some hours merely to as long as seven months. 

It is customary to attribute these subjective and objective 
changes to the fact of the various anastomoses between facial 
and sensory nerves, such as the rami communicantes with the 
auditory, the vidian nerve, the great superficial petrosal, the twig to 
the tympanic plexus, which runs in the connection between the otic 
ganglion and the glossopharyngeal, the chorda tympani, the posterior 
auricular branch which joins the great auricular from the cervical 
plexus, etc. In 4 out of 10 cases, MacCallan found a direct con¬ 
nection between the glossopharyngeal and facial nerves at the 
stylomastoid foramen. 

Yet this anatomical explanation is unsatisfactory. These anas¬ 
tomoses are more or less constant, whereas the sensory changes 
in facial palsy are not. When they occur, they ought to be much 
more pronounced than they often are. Further, occipital pain 
cannot be thus explained. 

The author is of opinion that, in many cases, the pathological 



process that has produced the facial palsy simultaneously affects 
the terminations of the trigeminal and of the cervical plexus and 
other sensory nerves. S. A. K. Wilson. 

(59) acute multiple Sclerosis (Encephalo myelitis periaxialis sclero- 
ticans.)] Marburg (Otto), Leipzig und Wien, 1906. 

A number of cases of disseminated organic disease of the nervous 
system have been recorded which, from their resemblance to dis¬ 
seminated sclerosis, both clinically and pathologically, may be 
described as acute or subacute multiple sclerosis. 

In a monograph of 100 pages, Marburg gives a review of the 
eases recorded in literature, and adds the reports of three which 
have come under his own observation. 

The disease occurs chiefly between the ages of 20 and 30. The 
symptoms indicate that there are multiple lesions in the brain and 
spinal cord; the onset is gradual; there is no fever; and though 
the affection is progressive, there is a tendency to remission and 
fluctuations in the symptoms. In the majority of the cases recorded, 
death occurred within three months—in some cases earlier, in 
some later. 

The author considers that this so-called acute multiple sclerosis 
is a form of true multiple sclerosis which is characterised by a 
more rapid course of the disease. The symptoms indicate that it 
is a form of multiple sclerosis, especially the mode of onset, the 
advance of the disease in stages, the remissions and intermissions, 
and the indications of multiple lesions. 

The pathological changes are characterised by degeneration of 
the medullar}' sheath of the nerve fibres, while the axis-cylinder is 
relatively intact. At the same time, or soon afterwards, there is 
proliferation of the neuroglia cells and of cells in the walls of the 
blood-vessels. The process is analogous to peri-axial neuritis. 

The pathological changes are inflammatory, and belong to the 
group of degenerative inflammatory changes. The nature of the 
degeneration of the medullary sheath of the nerve fibres indicates 
that it is due to a “ lecitholysis,” such as can be produced experi¬ 
mentally by “ ferment ” action. The pathological changes may be 
regarded as the result of a toxin. The final stage of the patho¬ 
logical changes is the complete replacement of the degenerated 
nervous tissues by a finely fibrillated neuroglia tissue, which con¬ 
tains only few nuclei. 

The affection is regarded by Marburg as a form of degenerative 
myelitis, ami he suggests for it the name of encephalo-myelitis 
periaxialis scleroticans. 



Three cases are recorded in detail, and eleven excellent illustra¬ 
tions of the histological changes in the nervous system are added. 

R. T. Williamson. 

ACUTE DISSEMINATE SCLEROSIS. (Uber akut verlaufende 
(60) multiple Skierose.) Karl Wegelin, Deutsch. Ztschr. fur 

Nervenheilk., Bd. xxxi., S. 313. 

Eduard Muller has shewn that the anatomical picture of dis> 
88 min ate sclerosis may be the final stage of quite different pro¬ 
cesses. For instance, he separates sharply the acute progressive 
condition following disseminated encephalomyelitis from the true 
scUrose en plaques, on both clinical and anatomical grounds* 
Wegelin describes a case, however, that shews the great difficulty 
of making this distinction. The patient was a man of 34 The 
first symptoms were parsesthesise and formication in both legs. 
Weakness followed, and within six weeks the paraplegia became 
absolute, both to motility and sensation, from the third rib down. 
There was at that time no other symptom except slight nystagmus. 
This state continued for three months; some of the sensory 
symptoms improved, but marked atrophy of the small hand 
muscles developed, with reaction of degeneration. Lumbar punc¬ 
ture showed on one occasion 52 cells to the, on another, 82 ; 
86 per cent, of the latter were lymphocytes. The patient, with 
broncho-pneumonia, died six months after the first symptoms. In 
the course of the latter, speech disturbances, paralysis of the right 
internal rectus and left facial and left hypoglossal made their ap¬ 
pearance, though only for two days, as they disappeared before 
death. At the autopsy, very typical patches of sclerosis were 
found disseminated through the brain and spinal cord, especially 
the latter. There was a large area from the first to third dorsal 
segment, becoming quite complete in the latter situation. The 
posterior columns, particularly the median, were especially affected. 
Vessel changes were slight and inconstant, differing thus from 
those described in most cases of acute multiple sclerosis. The 
writer considers that they were secondary. A detailed description 
of the sclerotic foci is given ; they differed in no single respect from 
the classical descriptions of the patches in disseminate sclerosis. 
The writer controverts Muller’s views as to the non-existence of 
true acute disseminate sclerosis, in detail, and regards his case as 
conclusive evidence of the existence of such cases. He considers 
that Muller’s grouping of all such cases under the title “ secondary 
sclerosis ” is arbitrary, as no distinction can be drawn between the 
acute and chronic cases. Ernest Jones. 



and Wolf, Joum. Amer. Med. Assoc., Dec. 29, 1906, p. 2138. 

A child, aged months, was admitted to hospital for meningitis. 
Forty-five c.c. of turbid cerebro-spinal fluid were removed under 
high pressure by lumbar puncture. The cellular elements were 
almost exclusively small mononuclear leucocytes. An organism 
was isolated showing all the characters of the diphtheria bacillus, 
including pathogenicity to guinea-pigs. Cultures from the nose 
and throat, which showed no evidence of inflammation, yielded 
staphylococci, streptococci, pneumococci, and bacilli resembling 
those isolated from the cerebro-spinal fluid. The autopsy revealed 
general miliary tuberculosis. Cultures from the heart blood, peri¬ 
toneal and pericardial fluids were sterile, but those from the 
meningeal fluid and exudate at the base of the brain yielded the 
same organism as that isolated from the cerebro-spinal fluid by 
lumbar puncture. 

The writers think that diphtheria bacilli occur more frequently 
in the central nervous system than is suspected, and that on careful 
search they could be found in a large number of cases. 

J. D. Rolleston. 

(62) SCLEROSIS. Joseph Collins, Joum. of Nerv. and Ment. Dis., 
Dec. 1906. 

Dr Collins describes a clinical picture of cases of cerebral arterio¬ 
sclerosis, where the cerebral arterio-sclerosis is the primary condi¬ 
tion, and in which no changes can be found in the skeletal vessels 
during life. He states that it forms a definite clinical picture 
upon which a diagnosis of the condition can be made. The 
patient complains of headache, varying in degree and character; 
he is subject to attacks of meaningless laughter, more rarely of 
crying, without attributable cause. The appearance of the patient 
is very striking, resembling that of a patient suffering from 
paralysis agitans, the immobility of the features is very marked. 
The gait is slow, limited, and shuffling. Mental symptoms come 
on later, marked by depression and apathy. The reflexes are 
active, Babinski’s sign is sometimes present. The arterial pressure 
is not necessarily high, and there is sometimes complete absence 
of visceral and skeletal arterio-sclerosis. 

Dr Collins describes two examples of the condition and believes 
it to be a not uncommon one. 



In the autopsies of these cases the chief change is found in the 
arteries of the brain. 

The brain shows shrinking as a rule, in other cases this is not 

The most striking changes are to be found in the middle 
cerebral arteries. Duncan Lorimer. 

(63) A HAEMORRHAGE. (Destruction d’trn peduncle c6r6belleux, 
etc.) A Porot, Rev . Neurolog., Dec. 15, 1906. 

A MAN aged 50, with an alcoholic history, had a sudden and 
severe attack of vertigo, without loss of consciousness. Vomiting, 
diplopia, inequality of the pupils (left greater than right), and 
slowing of the pulse were other early but transient symptoms. 
At the end of a week, a careful examination was made. The 
vertigo had lessened, but still reappeared on the slightest move¬ 
ment. The left knee-jerk, exaggerated at first, was now normal,, 
whilst the right was still active. Hearing was a little defective 
on the right side. In walking, the legs were kept wide apart, 
and there was a tendency to fall to the right. There were also 
present on the right side hemiataxia, liemiasynergia, and diadoco- 
cinesia; the actual power of the muscles of the right side was 
practically unaffected. 

The patient died of tuberculosis, and at the autopsy the nervous 
symptoms were found to be due to a haemorrhage destroying 
the right superior cerebellar peduncle at its origin from the 
cerebellum. Stanley Barnes. 

(64) CAL TRAUMA. (Die Arteriosklerose eine Folge des 
psychischen und physischen Traumas.) O. Watermann 
and Franz Ludwig Baum, Neurolog. Centralbl., Dec. 16, 1906, 
Jahrg. xxv., S. 1137. 

It has long been known that arterial changes, with accompanying 
high blood pressure, are frequently to be met with in neurasthenic 
and depressive states. The authors maintain, as a result of three 
years of observation, that the primary change in the vascular 
system is the raised blood pressure ; especially is this so in the 
case of the traumatic neuroses. This raised blood pressure leads 
to diminished extensibility and elasticity in the small arteries, 
with the ultimate production of arterio-sclerosis and its effects. 
They quote many authorities in support of this view of the 



mechanism of arterio-sclerosis. Their own opinion is that 
traumatic neuroses invariably produce this effect. This is based 
on the estimation of blood pressure in a large number of 
cases. Eight of these cases are shortly described. None had 
evidences of kidney or heart disease. None had been examined 
before the initial trauma. All had an average blood pressure, 
estimated on about twenty occasions, each by means of Gartner’s 
tonometer, about twenty millimetres above the usual. 

Ernest Jones. 

(65) BRAL TUMOURS. (Klinischer Beitrag zor Kenntnis der Hira- 
tumoren.) G. Mingazzini, Monaisschr. f. Psychiat. u. Neurol 
Bd. xix., H. 5, S. 442. 

Case 1. Tumour of the anterior part of the corpus callosum. —The 
patient, a man aged 52, a year and a half before coming under 
observation had a severe attack of vertigo, which recurred twice 
some months later. After the first attack, weakness in the arms 
(not in the legs) was noted, which varied in degree, but never 
entirely disappeared. Later, head pain, frontal and temporal, was 
complained of: vomiting and convulsions never occurred. When 
he came under observation, about three months before his death, 
there were no mental signs except some defect of memory. In 
hospital, the head pains were violent and constant, the motor dis¬ 
turbances steadily increased, and mental changes—marked apathy, 
general slowing of mentalisation and defective memory, without 
any hallucinations or excitement—appealed fairly rapidly, only a 
few weeks before death. There was marked double optic neuritis; 
the left side of the face, upper and lower, was paretic ; otherwise 
the cranial nerves were intact. There was no articulatory defect. 
The muscles of the neck were generally rigid and the head re¬ 
tracted. All limbs were weak and spastic, left much more so than 
right, and legs more than arms. Practically no ataxia of limbs; 
no sensory or trophic changes. Romberg’s sign was absent; he 
could not stand upright at all, and, when he tried, he tended to 
fall back, and to the right The left knee-jerk was active; the 
right could not be elicited ; there was no ankle- or knee-clonus; 
the triceps tendon reflexes were fairly active. Lumbar puncture 
showed enormous increase of cerebro-spinal pressure. The skull 
was trephined: no relief of symptoms. The autopsy disclosed a 
gliomatous tumour involving and evidently starting from the 
anterior half of the corpus callosum, and extending into the brain 
on either side—further on the right side than on the left—so as to 
implicate the upper part of the caudate nucleus, the internal 
capsule, and the lenticular nucleus. 



Remarks .—This case fully supports the view of Duret that bi¬ 
lateral hemiparesis, without implication of cranial nerves or sen¬ 
sory disturbance, is characteristic of tumour of the corpus callosum. 
On the other hand, the signs enumerated by Bristowe, and later 
by Ransom, as diagnostic of tumours in this region, receive but 
little confirmation. Thus, contrary to what they state, the general 
symptoms of cerebral tumour ( c.g . headache, optic neuritis, vertigo)- 
were very marked; the paresis appeared not in the form of a hemi¬ 
plegia, but in that of a paraparesis, affecting first the arms and 
much later the legs ; the mental condition of stupor developed not 
slowly and gradually, but rapidly, and there were never hallucina¬ 
tions or conditions of excitement; there was never any sign of 
twitchings or convulsions. Schuster gives, as the signs suggestive 
of a tumour of the anterior part of the corpus callosum, (1) develop¬ 
ment of mental disturbances long before any motor signs; (2) an 
isolated and early implication of one or both lower facial branches ; 
(3) rotation of the head to the paralysed side, and general con¬ 
tracture of the neck muscles; (4) greater paralysis of the arma 
than of the legs; and (5) a gait like cerebellar ataxia. Of these 
signs, Mingazzini’s case exhibited only contracture of the neck 
muscles and affection of the arms before the legs: possibly, the 
tendency to retropulsiou should also be included, as it occurs in 
certain cerebellar lesions. 

Mingazzini, therefore, concludes that the symptomatology of 
callosal tumours is still so doubtful that one cannot venture tn 
make a certain diagnosis in any individual case: at present, wo 
can only collect facts. Even the anatomy of the corpus callosum 
is but little known: thus, it is still an unsolved problem why, 
when the callosal fibres degenerate in their course within the 
corpus callosum, the degeneration stops abruptly there, and does 
not extend to the hemispheres (Mingazzini’s observation). 

Clinical evidence (obtained from cases of tumour and of con¬ 
genital absence of the corpus callosum), supported by experimental 
results, leaves no doubt, Mingazzini thinks, that the motor 
phenomena seen in cases of tumour of the corpus callosum are due 
exclusively to involvement of the pyramidal fibres in the internal 
capsule and lenticular nucleus, not at all to disease of the callosal 
fibres : the extent to which the centrum ovale is invaded or com¬ 
pressed by the tumour on one or both sides will determine tho 
distribution of the paresis in any case. 

Similar evidence leads him to reject the view of Schuster that 
mental disturbances are a direct symptom of a lesion of the callosal 
fibres, dementia (sometimes combined with a state of excitement), 
of lesions of the anterior part, and conditions of delirium in lesions 
of the posterior part. Schuster explains the absence of mental 
symptoms in certain recorded cases of agenesia of the corpus- 



callosum on the ground of functional compensation by other 
systems: this cannot be accepted, as compensation could be 
effected only by the anterior commissure, and this has not once 
been found abnormally developed in such cases (Bianchi). 

Case II. Tumour in the upper part of the left central convolu¬ 
tions .—The patient was a man aged 26. Three years previously, 
slight irritability of temper had appeared—the first sign; soon 
headache followed, chiefly frontal, and vomiting when the head 
pain was violent. No other symptom was noted for about two 
years, when he had attacks of temporary numbness of the right 
leg (“ sensory epilepsy ”), followed in a short time by paresis of the 
same leg, especially of the foot, which gradually diminished but 
never entirely disappeared. Soon thereafter, clonic spasms of 
the Jacksonian type occurred, which were at first limited to the 
right leg, but later spread to the arm and face of the same side. 
Consciousness was lost in only one attack, which affected mostly 
the right side of the body and which was followed immediately by 
complete paralysis of the right leg; this gradually improved until 
only the muscles of the right foot were paralysed. 

The chief points noted, less than a year after the onset of 
sensory epilepsy, were: No obvious mental symptoms; tender¬ 
ness of the cranium, especially over the middle and upper parts of 
the left central convolutions; marked optic neuritis, greater on 
the left side, and paresis of right lower face—otherwise cranial 
nerves intact; paresis of right arm, without rigidity; flaccid 
paresis of whole right leg, with total loss of movements of foot; 
right knee-jerk much exaggerated, right ankle clonus, absence 
of Babinski’s sign; no gross sensory changes. 

Tumour of the upper part of the left central convolutions was 
diagnosed and found at operation; a glioma, the size of a tangerine, 
affecting cortex and sub-cortex of this region, adherent to the 
superior longitudinal sinus and extending to the free margin of 
the hemisphere, was removed ; death occurred six days later from 
hemorrhage and consequent diffuse encephalitis. 

Attention is drawn to several points. (1) The first symptom 
noted was slight irritability of temper, which involved the patient 
in difficulties; Mingazzini thinks that this defect of self-control 
was a direct result of the incipient disease, and that this considera¬ 
tion is a point of medico-legal interest and importance, not 
sufficiently recognised. (2) The early appearance of sensory 
epilepsy, viz. attacks of numbness in the right leg. (3) The 
occurrence of monoparesis (right leg) before signs of Jacksonian 
epilepsy; this is not the rule, indeed it is rare in tumours of the 
central convolutions (Oppenheim); the explanation may be either 
that the tumour began in the sub-cortex and later spread to the 



cortex, or that a sudden haemorrhage occurred early in the growth 
of the tumour. (4) The rare occurrence of such a limited crural 
monoplegia in a lesion of the central convolutions—at one stage, 
after the severe convulsive attack, paralysis was limited to the 
right foot; this affords confirmation of the contention of Bruns 
that paralysis is a more certain localising sign of a lesion in this 
region than the Jacksonian attacks are. 

A. W. Mackintosh. 


(66) CEREBELLAR ATAXY OF CHILDREN. (Familiars para- 
lytisch-amaurotiscbe Idiotie und famili&re Eleinhirnataxie des 
Kindesalters.) H. H icier, Deutsch. Ztschr. far NervenheHk ., 
Bd. xxxi., S. 231. 

The writer recorded nine years ago two cases of Leber’s optic atrophy 
in Jewish brothers. Since then no other sign of nervous affection 
has developed in them. He now publishes an account of a brother 
and sister of these former patients. The girl, aged nine, whose 
first symptom dates to the age of four, had on examination speech 
defect, cerebellar inco-ordination, tremor, spasticity, Babinski’s 
sign, increased knee-jerks, optic atrophy, nystagmus, and mental 
deficiency. The boy, aged thirteen months, was perfectly well for 
the first seven months of his life ; the first symptoms were apathy 
and gradual uselessness of his muscles. At present he rarely 
moves his arms and never his legs. The muscles are flaccid, but 
the deep reflexes are much exaggerated. Blindness is present. 
There is double optic atrophy ; at the macula is a white area twice 
the size of the disc and having in its centre a cherry-red spot. 
The boy is thus a typical case of the Tay-Sachs disease, while the 
girl’s case should be counted as a heredo-cerebellar ataxy (of 
Marie). Three hereditary diseases thus occur in four children of 
the same parents. The writer then embarks on some theoretical 
speculations, the main thesis of which is the substantial unity of 
all hereditary diseases of the nervous system. 

Ernest Jones. 


THE BLOOD PRESSURE. (Ein fall von progressiver Para¬ 
lyse mit gehfiuften epileptiformen Kr&mpfen nebst Beobach- 
tungen fiber das Verhalten des Blutdrucks bei solchen 
Anf&llen.) W. Plaskuda (of Uckermunde), Allg . Ztschr. f. 
Psych., Bd. 63, H. 2. 

The author measured with the Riva-Rocci apparatus the blood- 
pressure of a general paralytic immediately before and after 



attacks. Just before the attack the pressure rose somewhat, but 
at the moment when general convulsions began the pressure fell 
about 10 mm.; during the convulsion the pressure could not be 
definitely measured, but it apparently rose suddenly with the con¬ 
vulsion and persisted for a few minutes after the rigidity had 
passed off and then gradually fell. C. Macfik Campbell. 

(68) Gowers, British Medical Journal , Dec. 8, 1906, p. 1617. 

This is the third lecture on the subject. (See Rev. of Neurology 
and Psychiatry , Vol. iv., pp. 696 and 697.) The writer acknow¬ 
ledges that the term “ migraine ” has lost its original significance of 
hemicranial pain and is now applied to all forms of paroxysmal 
headache. He maintains that migraine and epilepsy are closely 
related, as is shewn by their alternation, by the occurrence of one 
condition when the other is relieved, and by the occasional cases 
in which the same premonition may usher in either one or the 
other attack. The clinical resemblances of the two conditions and 
theii differential diagnosis are next dealt with. In the worst cases of 
migraine an ancestral history of gout is rarely absent; in epilepsy 
the ancestors have suffered from epilepsy or insanity. The sensory 
aura of migraine practically never lasts less than five minutes, 
and rarely less than fifteen. Its characteristic feature of gradu¬ 
ally ascending the arm, leaving numbness behind it, is never seen 
in epilepsy. It may affect both hands; it never affects the foot, 
and rarely the lower limb; it never passes down the trunk nor up 
to the face and head; it is occasionally felt in the lips and even 
the tongue simultaneously with the arm. In all these points it 
differs from epilepsy. The visual aura of migraine is also longer 
that that of epilepsy. The dimness of sight is blotchy, irregular, 
or one-sided, and is prolonged; in epilepsy it is general and 
momentary. A single flash of light, or multiple momentary bright 
“ stars,” so common in epilepsy, are not known in migraine, nor 
are the elaborate visual sensations of a scene, face, etc. The 
auras of migraine may occur with no succeeding headache; tem¬ 
porary aphasia may accompany them, as may a vague sense of 
giddiness. The severe and lasting pain commonly met with in 
migraine never occurs in epilepsy, nor is the pain of epilepsy one¬ 
sided. Vomiting may occur after both conditions, but immediately 
in the case of epilepsy, and only after some hours in the case of 
migraine. Other effects of the pain of migraine may be stupor, 
somnolence, delirium (followed by amnesia), and loss of conscious¬ 

In the treatment of migraine the writer recommends continued 
administration of nitroglycerin combined with strychnine. 

Ernest Jones. 



POST-DIPHTHERITIC EPILEPSY. Dodson, Archives of Pediatrics , 
(69) Aug. 7, 1906, p. 626. 

A GIRL, aged 10, in the second week of diphtheria developed slight 
spasms, which first appeared in the right arm, and soon became 
general. They rapidly increased in frequency and severity, until 
in a few days she was having forty to fifty grand mal seizures in the 
twenty-four hours. The spasms disappeared within three or four 
weeks, and the child made a perfect recovery, and never had any 
trouble of the kind subsequently. 

The epileptic seizures are attributed by Dodson to a special 
selective action of one of the toxines of diphtheria on the cortical 
cells. J. D. Rolleston. 

( 70 ) caption de l’hystdrie et de lliypnotisme. Babinski, Arch. gin. 
de mid., Aug. 28, 1906, p. 2187. 

Hysteria manifests itself in two distinct groups of symptoms, of 
which the “ stigmata ” are more or less permanent, the others are 
transitory. The stigmata, in addition to their fixity, usually 
develop without the patient’s knowledge, and include pharyngeal 
anaesthesia, hemianarthria, unilateral impairment of the special 
senses, in particular vision, with concentric restriction of the visual 
field, monocular diplopia or polyopia, dyschromatopsia for blue 
and violet, red remaining normal; in addition, one might mention 
points douloureux, clavus, etc. Fits or attacks, paralyses, con¬ 
tractures, aphonia, mutism, etc., constitute the transitory symptoms, 
which often appear suddenly under the influence of some emotion, 
and sometimes disappear with equal suddenness. 

Babinski, however, has found in a wide experience that certain 
modifications of the classical description are necessary, a conclusion 
frequently arrived at by observers of other generations and of our 
own. The so-called permanent symptoms may one and all dis¬ 
appear under suitable treatment. They are the result of auto¬ 
suggestion in many cases, or rather of the unconscious suggestion 
of the examining physician, as Bernheim of Nancy has long main¬ 
tained. The method of examination of the patient is frequently 
sufficient to evoke in his mind the idea of a hemianresthesia, or of 
a visual affection. By carefully studying the best way to conduct 
an examination, Babinski has found that in not one single new 
case of hysteria coming under his observation was hemiansesthesia 
present. Identical results were obtained in regard to restriction 
of the visual fields. If the patient had not been examined before. 



no alteration was forthcoming. It cannot therefore be said that 
the stigmata of hysteria are either constant or permanent, and 
therefore any definition based on their presence is likely to be 

Babinski draws an important distinction between suggestion 
and persuasion. Suggestion signifies the action by which we 
endeavour to make someone accept or realise an idea which is 
manifestly illogical. To tell someone whose muscles are function¬ 
ing normally that he is hemiplegic or paraplegic is to suggest: but 
to declare to a patient with functional paralysis that he will get 
better as the result of treatment is to persuade. 

The definition which the author proposes is couched in the 
following terms:— 

Hysteria is a particular psychical state which is capable of 
giving rise to certain conditions which have features 
of their own. 

It manifests itself in primary and in secondary symp¬ 

The former can be reproduced exactly by suggestion in 
certain subjects, and can be made to disappear under 
the sole influence of persuasion. 

The secondary symptoms are in direct relation to the 
primary ones. 

Conformably to this definition, Babinski excludes from the category 
of hysteria any symptom which cannot be reproduced by sugges¬ 
tion. It is impossible to evoke nervous attacks associated with 
lividity of the lips and followed by cutaneous ecchymoses: these 
cannot therefore be hysterical. The exaggeration of deep reflexes 
and the occurrence of “ spinal epilepsy ” cannot be produced by 
suggestion: these cannot therefore be hysterical. For the same 
reason he thinks that hysteria can never give rise to paralysis 
limited to the domain of a peripheral nerve. And so on. Numer¬ 
ous conditions which have been considered hysterical must be 
excluded from a disease which has been too comprehensive. 

Babinski’s conception of hypnotism is that it is a psychical 
state which makes the subject of it susceptible to suggestion from 
without. It is manifested by phenomena arising from suggestion, 
which can be made to vanish by persuasion, and which are identical 
with hysterical phenomena. 

There is therefore no difference between the one condition and 
the other, except in so far as that auto-suggestion may produce 
hysterical conditions, whereas the question of auto-hypnotisation 
is problematical. Resort should be made to hypnotism solely in 
cases which are rebellious to ordinary methods of treatment. 

S. A. K. Wilson. 




(71) et la nature de lTiysWrie.) Sollier, Arch. gin. de mid., Oct. 9, 
1906, p. 2585. 

In this communication Sollier proceeds to examine critically the 
theory of Babinski on the nature of hysteria. He maintains that 
the latter’s definition of the disease is a pctitio principii. It is 
equivalent to the following paralogism: “ The troubles which can 
be reproduced by suggestion in certain subjects are hysterical; 
now, various symptoms noted in cases of hysteria can be repro¬ 
duced by suggestion in certain subjects and made to disappear by 
persuasion, therefore only those troubles are hysterical which can 
be reproduced by suggestion and banished by persuasion.” In 
other words, hysterical symptoms can be reproduced by suggestion 
and made to disappear by persuasion because they are . . . hys¬ 
terical. Babinski’s definition appears to the author to offer two 
terms for explanation, only one of which is defined. He proceeds 
to pass various criticisms on Babinski’s theory. The latter cannot 
regard hemiansesthesia as a fixed stigma, because he has often 
fouud it absent (when tested by a strong faradic current) in 
patients to whom the idea has not been suggested by a badly- 
conducted examination. Sollier emphasises strongly the existence 
of most varying degrees of heraiamesthesia which certainly escape 
notice if tested by strong electricity. Sensitiveness to electricity 
is often present in cases of hysteria when other forms of stimulus 
evoke no response. 

Further, why should amesthesia be suggested to the patient by 
an awkward examination ? Why not hyperesthesia 1 An associa¬ 
tion of normal cutaneous resthesia with anesthesia of deeper tissues 
is by no means uncommon. That many of the symptoms of the 
hysterical subject are unknown to him until demonstrated by the 
physician appears certain. Of various visceral anomalies it is 
indeed singular that they always consist in modifications of 
amesthesia. An hysterical patient who complains of anorexia 
and gastric pain has usually a degree of cutaneous amesthesia over 
the hypogastrium. If this were the result of suggestion, why 
should it not be hyperesthesia ? 

If a condition does not disappear under the influence of persua¬ 
sion, we have no right to assume that it cannot be hysterical. Sollier 
has seen bullae of pemphigus appear in a few hours in a hysterical 
paraplegia under the influence of intense emotion, and disappear 
with improvement in the other symptoms, yet Babinski excludes 
all such phenomena from the category of hysteria, “ because they 
cannot be reproduced by suggestion.” 

According to Sollier, hysteria is due to inhibition of the func¬ 
tions of the cerebral cortex : variations in degree and extent of this 



inhibition explain the variability of hysterical phenomena. Since 
cortical centres have a double function, psychical and sensori¬ 
motor, hysterical phenomena may be accompanied by sensory, 
motor, visceral, or psychical disturbance. S. A. K. Wilson. 

(72) (Ueber Farbensehen und Farbenblindheit bei Hysteria.) L. 

Bregman, Neurolog. Ceniralbl., Dec. 16, 1906, Jahrg. xxv., 
S. 1143. 

Dyschromatopsia is a fairly frequent symptom in hysteria. The 
earliest indication is a concentric retraction of the visual field, most 
for green and violet, then for red and orange, least for yellow and 
blue. This colour affection in worse cases goes on to colour¬ 
blindness, usually partial, but occasionally total. 

The reverse of this condition, namely, the colouring of the 
field with a particular hue, is much rarer. The colours that occur 
are yellow, red, green, blue, in this order of frequency. 

A combination of the two conditions must be extremely rare, 
for Bregman can find no record of any case similar to the one he 
now publishes. The patient was a soldier, aged 30, who in the 
Japanese campaign incurred a traumatic hysteria. The symptoms 
of this are described, and the eye manifestations detailed. All 
objects seemed to the patient to be tinted yellow. With the wool 
tests red and green were recognised when saturated, but were 
called yellow when pale; white was called yellow, and both blue 
and black were called black. There was concentric retraction of 
the fields, most for blue, least for yellow. The author calls atten¬ 
tion to the fact that the fundamental changes, yellow vision and 
blindness for blue, relate to complementary colours. He attributes 
this to an excitation state of the cortical area concerned with 
yellow, with a corresponding depression in that concerned with 
the complementary colour. 

In a second case, that of a soldier, aged 25, all objects appeared 
as tinted with red. With the right or worse eye no other colours 
could be distinguished; with the left eye all colours could be 
distinguished in spite of their suffusion with red. There was no 
contraction of the fields. 

The author refers to his researches on coloured vision in 
tabetics, which differs from that of hysterics in the following 
particular. In tabes the field is tinted with green and violet— 
when an object is first looked at it appears green, then late violet. 
The green appears in sharply defined patches, the violet in vague 
clouds, neither affecting the whole field. They are evanescent 
phenomena, usually lasting over ten minutes in attacks; while in 



hysteria the condition is more permanent. In tabes there is 
diminished acuity of vision for the two affected colours; in 
hysteria for the complement of the affected colour, though as this 
occurred in only one case it is not safe to generalise about it 

Ernest Jones. 

A CASE OF HYSTERICAL FEVER. (Ein Fall von hysterischem 

(73) Fieber.) Goldflam, Neurolog. Ceniralbl., Nov. 1, 1906, p. 978. 

Goldflam’s case was observed as long ago as 1890, and concerns 
a girl of sixteen, with symptoms leading to a diagnosis of osteomye¬ 
litis of the ulna, and to two operations. No sign of disease of bone 
or marrow was found, but during the whole course of the illness 
her temperature fluctuated daily, as in pyaemia, from subnormal 
to 104* F., or higher. After the operations her case was referred 
by the surgeon to the reporter, who discovered general analgesia, 
with the exception of the face, anaesthesia and “ areflexia ” of the 
mucous membranes, left-sided ovarian tenderness, exaggerated 
knee-jerks, and pronounced concentric diminution of the visual 
field. At a later stage the patient gave unmistakable indications 
of having tampered with her operation wound and with other 
parts of her body: in short, she was a case of hysteria mutilans. 
That the temperature was genuine admits of little doubt, for the 
continued observation of the physician prevented any manoeuvring. 
Further, the author thinks that profuse sweating, which occurred 
in her case with each fall of temperature, could not be simulated 
voluntarily. It should be said that the operation wounds remained 
clean throughout and healed by first intention. 

There are numerous references to the literature. 

S. A. K. Wilson. 

(74) vec (Prague), Rev. Neurolog., Dec. 15, 1906. 

Under this heading the author gives a clinical description of a 
fairly typical case of Dercum’s disease. The patient was a woman 
of 60, of a remarkably neurasthenic type, and with an enlarged 
thyroid, in whom the symptoms had been coming on for about ten 

The author discusses the diagnosis and causation, suggesting 
that some “ functional lesions ” of the thyroid, genital, or other 
glands may have played some part in causing an auto-intoxication. 

Stanley Barnes. 



the relation of school work to the mental fatigue 

(75) OF CHILDREN. B. Sachs (New York), Joum. of Nerv. and 
Ment. Dis., Dec, 1906. 

In connection with the effect of school work on the nervous dis¬ 
orders of childhood, the author writes strongly condemning the 
too hasty conclusions arrived at by the pedantic application of 
psychologic methods to this matter, and further exploited by writers 
in popular magazines. He states that, after an experience of twenty- 
one years, and after studying thousands of cases in private and 
hospital practice, he has never once seen an instance of serious 
injury done to a child’s mental development by any influence of 
school as such. 

Dr Sachs further points out the immense improvement that 
has taken place in the methods of teaching in the present day. 
He recognises the fact that mental fatigue is just as normal and 
to be expected as physical fatigue, that is, when it is transitory, 
and promptly recovered from after a period of rest. 

In speaking so strongly, Dr Sachs is careful to point out that 
there are naturally many cases in which the particular child 
is unfit for the life of the school, but he insists that the school 
must be arranged for the benefit of normal children, and not 
for the unfit and mentally deficient. 

He then points out the great importance of establishing special 
schools for those children not quite equal to ordinary school life. 
Dr Sachs is more inclined to blame the generally restless and 
hurried spirit of American life as the cause of the functional 
neuroses of childhood, and he credits the school with effecting a 
quieting and beneficial effect on children. Duncan Lorimer. 

APHASIA AND DIA80HISI8. Yon Monakow (Zurich), Neurol. 

(76) Centrcdbl. , Nov. 16, 1906, p. 1026. 

This paper is an important contribution to the study of the 
question of aphasia. The author admits that the more closely the 
clinical phenomena presented by patients with aphasia are ob¬ 
served, and the more accurately the anatomical changes are 
examined, the greater is the difficulty of furnishing a satisfactory 
explanation of the connection between the site of the lesion and 
the symptoms of aphasia as observed during life. Even with re¬ 
gard to the coarser localisation of aphasia, there are many and by 
no means inconsiderable contradictions. The number of negative 
cases, for instance, is much larger than is usually admitted. Still 
larger is the number of those cases in which, in spite of the per- 



sistence or the increase in size of the lesion in the speech region, 
the aphasic symptoms disappear: and further, the number of cases 
is very great in which the aphasic symptoms persist for an un¬ 
usually long time, although the lesion is beyond the limit of the 
speech region. Paradoxical cases also, such as sensory aphasia 
with destruction of Broca’s convolution, and motor aphasia with 
the lesion in the temporal lobes, are by no means exceptional; and 
again, the anatomical conditions for the causation of special forms 
of aphasia, such as subcortical or transcortical, are in no degree 
uniform. Finally, the variety as regards affections of intellect 
shown in cases in which the site of the lesion and its relation to 
the surrounding parts are quite similar is very striking. 

The author shows that the results of his own special observa¬ 
tions indicate that mere interruption of continuity of the fibres is 
by no means sufficient to explain the varieties of form in aphasia 
and other allied disturbances. We must lay greater weight than 
hitherto upon the nature of the disease, the mode of its appearance, 
and the accompanying circulatory, mechanical, toxic, and other 
factors. It is not admissible, according to him, to attribute the 
various special groups of aphasia, as is done by Wernicke’s school, 
simply to the interruption or disappearance of certain bundles of 
fibres or parts of the cortex. He examines and rejects the theory 
which explains the rapid recovery of speech, in spite of the persist¬ 
ence of the lesion, by the vicarious assumption of the duties of the 
special centre by other unaffected areas of the cortex. He points 
out that it is unreasonable to expect that cortical areas, which al¬ 
ready have enough to do in the discharge of their own special 
functions, should in their more or less impaired condition under¬ 
take new and complicated duties, such as those of speech. He 
insists that in order to obtain a firm physiological basis for the 
localisation of speech, it is necessary to determine accurately— 
(1) what symptoms must be produced under all circumstances by 
a purely mechanical destruction of various parts of the speech 
region ; and (2) what lesions can produce the more inconstant and 
temporary aphasic phenomena. 

The author draws attention to a special form of action-at-a- 
distance (Fernwirkung), to which he applies the term diaschisis. 
He distinguishes this from the effect of circulatory disturbances, 
irritative disturbances due to the products of the disease, or of 
mechanical, toxic, and other conditions in the neighbourhood, 
and he defines it as the temporary suspension of function which 
arises from the local interruption or disturbance of a tract of fibres 
which directs or carries out the function of a neighbouring part. 
Such a suspension of function may arise from the interruption of 
projection or association fibres in such a way that secondary 
centres, not in themselves directly involved in the lesion, but 



connected through fibres with the part involved, are not stimu¬ 
lated from the centre which has been destroyed. The paralysis or 
abnormal activity thus produced in associated centres not in 
themselves directly affected, but which under normal conditions 
act in association with the primary centre of which they are only 
relatively independent, constitutes diaschisis. These secondary 
associated centres may lie at a distance from the primary one. 
Where the secondary centres are comparatively independent, they 
will correspondingly soon recover their activity; while those 
symptoms which are directly produced by the injury to the fibres 
derived from the affected area alone remain. 

As an example of diaschisis may be quoted the disappearance 
of the spinal reflexes on the paralysed limbs immediately after an 
attack of hemiplegia. In a similar way may be mentioned the 
bilateral disappearance of knee-jerks in cerebellar disease, in com¬ 
pression of the medulla, and in complete transverse division of the 
spinal cord. In none of these conditions is the loss permanent, 
but in all it is due to an interference with higher centres which 
are physiologically associated with the parts involved. In like 
manner aphasic symptoms are in the beginning partly those which 
are permanent and partly those which are of a more or less tem¬ 
porary character. In small, sharply-defined traumatic foci in the 
speech area, even if bilateral, the permanent symptoms hardly ever 
contain a psychical element. They are more limited in character 
and involve simply the mechanism for the direct production of 
speech. Thus in lesion of Broca’s convolution, they would involve 
slowing of speech, difficulty in forming words, hesitating speech, 
and in severer cases complete word-dumbness without agraphia. 
Lesion of Wernicke’s convolution would be accompanied by diffi¬ 
culty of speech, paraphasia, logorrhoea, jargonophasia, perseveration 
(senseless repetition of words), and, when the lesion is bilateral, 
cortical word-deafness. In such cases the temporary associated 
symptoms would be those usually called transcortical, e.g. disturb¬ 
ance of the complicated process of “ Klang-evocation,” the power 
of understanding the sense of a word, or of arranging words into 
sentences, loss of knowledge of relation between word and object, 
loss of the finer components of written speech, partial disturbances 
of orientation in time and place, and even many disturbances 
of intellect in so far as they are connected with speech. Such 
“transcortical” symptoms can only be caused by the elective 
injuries of diffuse and very complicated associated systems, i.e. of 
paths which are themselves slightly or not at all anatomically in¬ 
jured. These transitory symptoms, in so far as they are not 
“neighbour-symptoms,” or due to allied circulatory disturbances, 
are usually produced by diaschisis. It is clear that the degree of 
diaschisis will vary in different cases. In some cases diaschisis 



may be absent, and in others so many arcs may be injured that 
their activity cannot be re-established. Symptoms of aphasia then 
may depend more on the diaschisis in distant regions of the brain 
than on the local lesion itself. This mode of localisation involves 
that in each special case of aphasia there must be a definite local 
lesion; but this is not sufficient of itself to produce the symptoms 
unless it acts in distant associated parts by diaschisis. Besides the 
local factor, subordinate and accessory factors, such as the general 
nutrition of brain, circulation, nature of disease, etc., must be taken 
into consideration. The extent and the greater or less permanence 
of the temporary symptoms will depend on various factors, such as 
general functional conditions and power of recovery of the cerebrum. 

In this view the stabile forms of so-called cortical aphasia will 
be regarded as being caused by the destruction of Broca’s convolu¬ 
tion combined with various diaschisis effects which the brain may 
not be able to overcome entirely. But if, on the other hand, in 
spite of great extent of original lesion there is more or less com¬ 
plete recovery of speech, this depends not on vicarious interven¬ 
tion or education of corresponding convolutions of the other side, 
or any other part of the cortex, but from a retrogression of the 
original diaschisis. In completely negative cases we must assume 
absence of all diaschisis in an otherwise normally active brain. In 
such cases there must no doubt remain slight residual disturbances 
which can only be discovered by fine methods of investigation. 

The conception of diaschisis shows that for the mechanism of 
speech much more extensive cortical areas are involved than has 
been hitherto assumed, but that the speech function can be easily 
affected by injury to certain sharply localised groups of bundles and 
cortical areas by diaschisis. This is to be explained by preformed, 
extensive cortical innervation paths, but such local anatomical 
“ nodal ” points are not therefore to be regarded as special work¬ 
shops for speech. Thus a speech centre would simply be a locus 
minoris resistentia. In every case of interruption of these paths 
for speech innervation, there will therefore be a danger of their 
activity being temporarily affected. With a local lesion and an 
otherwise sound brain, the greater part of the loss of speech will 
in a short time be recovered from. 

The author hopes that the principle of diaschisis will be of assist¬ 
ance in clearing up our views as to the mode of action of cerebral 
lesions on the function of speech. Alexander Bruce. 

(Montreal), Joum. of Nerv. and Ment. Dis., Dec. 1906. 

In an article on the state of the fields of vision in lesions aflf ctingf 
the optic system, the author begins by a short account of the 



most recent views on the anatomy of the region. He traces back 
the macular fibres, and discusses their ultimate distribution. He 
further points out the comparative unimportance of the pulvinar 
and anterior corpora quadrigemina in regard to vision, as compared 
with the external geniculate body. He then discusses the question 
of the cortical representation of the retina in the occipital lobe, 
and reviews the opinions on this matter. 

A knowledge of their anatomical relations is of extreme 
importance in regard to cerebral localisation, from the clinical 
conditions. “ The fields and the acuity of vision vary very 
materially, according as the lesion affects the optic nerve tract 
or the radiations.” 

Dr Russel then gives accounts of six cases of lesions in the optic 
system, with a description of the clinical symptoms, the state of 
the optic discs, and the alterations in the fields of vision. In two 
of these lesions (chiasmal), a tumour of the pituitary gland was 
found, which was operated on by Sir Victor Horsley. The other 
cases were examples of lesions in different parts of the optic system, 
and showed correspondingly different clinical manifestations. 

Duncan Lorimer. 

mams’ NYSTAGMUS, a. Christie Reid, Brain , Vol. xxix., 
(78) 1906. 

The theory of the causation of miners’ nystagmus which has 
received most general support is that of Mr Simeon Snell, which 
makes it out to be a myopathy induced by chronic fatigue of the 
muscles, produced by working in a strained position. On this 
theory, defective illumination is only of subsidiary importance. 
Such a theory separates miners’ nystagmus from certain other 
forms of the disease which would naturally seem to be closely 
allied to it, such as the nystagmus which comes as the result of 
comeal opacities developing in early childhood, and any theory 
which might lead to the correlation of these different forms will 
naturally be examined in a spirit of benevolent criticism. An 
attempt to arrive at some such theory is given by Dr Reid in his 
interesting paper. He points out, to begin with, that much 
evidence has been adduced to show that insufficiency of light is 
the more important factor, and strained position of the eyeballs 
the less important His theory is “ that the affection is due to a 
disturbance of the centres having to do with the equilibration of 
the eyeball.” With dark adaptation the superiority of visual 
acuity in the fovea disappears; in fact, becomes lower than the 
rest of the retina. This is a factor of prime importance. Dr Reid 
next points out the close interdependence of equilibration of the 
eyes with equilibration of the body. In a miner’s life both those 



factors are met with. There is dim illumination and a constant 
tendency to disturbances of body equilibrium. Thirdly, there is a 
more or less rhythmical series of movements performed by body 
and head with eyes fixed. These, he considers, tend to produce 
the rhythmicity in character of the nystagmus. The onset is 
usually precipitated by debilitating influences of any kind. 

Leslie Paton. 


(79) MOVEMENTS OF THE SHOULDER. (Myopathie par 
Sursauts Deltoidiens pendant les mouvements de l’dpanle.) 

Guermonprez, Gas. des Hop., Oct. 11, 1906, p. 1383. 

A case illustrative of the errors likely to occur in the awarding 
of compensation to workmen for injuries sustained at their em¬ 
ployment. A mill-worker suffered from weakness and cracklings 
of the right shoulder, supposed to be due to a sprain sustained at 
his work; but on inquiry it was found that no real sprain had 
occurred, and on examination it was discovered that both 
shoulders were affected, that the cracklings only occurred when 
the arms were in a certain position, and that their seat was the 
deeper part of the deltoid muscle. There was no connection 
between these muscular jerkings and any sprain or other injury, 
and it was merely a coincidence that the crackling had been first 
noticed while the man was engaged at his work. 

Henry J. Dunbar. 


(80) SPINAL OORD. (Schweissanomalien bei Ruckenmarkskrank- 

heiten.) H. Higier, Neurol. Centralbl., Nr. 1, 1907, p. 19. 

The author, who published an article in the Deutsche Ztschr. f. 
Nervenheilk., Nr. 20, 1901, entitled, “ Zur Klinik der Schweiss¬ 
anomalien bei Poliomyelitis anterior (spinale Kinderlahmung) und 
posterior (Herpes zoster),” is of opinion that anomalies of sweat 
secretion, such as anidrosis, hyperidrosis, and paradoxical sweat 
secretion, would be much more frequently discovered and used 
for diagnostic purposes if they were searched for and duly con¬ 
sidered. According to him the central origin of sweat secretion 
is located on each side of the cortex, and connected with sub¬ 
sidiary centres in the medulla oblongata, where the principal centres- 
for the four extremities are found. The spinal cord contains 
throughout almost its whole length either centres or fibres for 
sweating. He records four cases of sweat anomalies. (1) A 
case of a sudden paralysis of the lower extremities, associated 



with an increasing optic neuritis, which produced bilateral 
amaurosis. On using means to induce sweating, it was found 
that the lower, paralysed part of the body remained practically 
perfectly dry, while the remainder of the body perspired profusely. 
(2) A man of forty-one years of age, in whom a fall from a con¬ 
siderable height was followed by a flaccid motor paralysis of the 
lower extremities, with loss of sensibility, especially for pain and 
temperature, with muscular atrophy, weakness of the tendon 
reflexes, and loss of the lower organic reflexes. The lower half 
of the body was found to remain perfectly dry, when profuse 
perspiration was present in the other half. (2) A woman of 
fifty-two, who had suffered for twenty-five years from progressive 
weakness in the right hand. She showed a right claw-hand, dis¬ 
sociated disturbances of sensibility in both upper extremities and 
the right half of the face, and indications of bulbar paralysis. 
There was loss of sweating on the right arm and the right 
half of the trunk. Case was probably one of syringomyelia, 
extending upwards and downwards from the cervical enlarge¬ 
ment (4) A man of forty-eight, from whom a malignant left 
kidney had been removed five months previously. Suffered for 
nine months from a flaccid paralysis of the lower extremities, 
which was first painful and later painless, in which there was 
loss of all the reflexes, deep and organic, and loss of sensibility in 
the legs, with bed-sores on the sacrum, absorption from which had 
produced a severe sweating in the face and the upper part of the 
body, but left the lower extremities and the lower half of the 
trunk entirely dry. 

The author points out that the secretion of the sweat glands 
is not to be regarded as a mere physical process of filtration, 
brought about only by an indirect influence of the nervous 
system through vaso-dilatation. He offers no opinion as to 
whether the centres are situated in the anterior horn near the 
motor ganglion cells, or at the basis of the posterior horns. 
He shows that the paths for the secretory nerves may be inter¬ 
rupted either in their peripheral course or in the sympathetic 
chain in the intra-vertebral ganglion, or, finally, in the grey 
matter of the spinal cord or in the cerebral cortex. 

In the paper published by the reviewer and Dr Pirie in the 
January number of this Review, the opinion is expressed that the 
spinal centres for the sweating fibres of the lower half of the 
body are probably situated in the intermedio-lateral cell-system 
of the lower dorsal and upper lumbar segments of the cord. The 
writers agreed with Higier in thinking that the loss of sweating 
depends directly upon the destruction of special centres for the 
function, and not upon any indirect influence of vaso-motor or 
vaso-dilator fibres. Alexander Bruce. 



(81) VERTEBRAL ANKYLOSES. (Pathogenic des Ankyloses- 
et particnli&rement des ankyloses vertdbrales.) Andr£ Leri, 
Congrts de Lyon, Aug. 2-7, 1906. 

This monograph concerns itself solely with true osseous ankylosis 
of the vertebral column, but the general etiology of osseous 
ankylosis in any part of the body is first summarised, and the 
importance of ossification as a secondary and compensatory factor 
in the “ functional adaptation ” of diseased or injured joints is 
emphasised. Local vertebral ankylosis is much more common 
than general, and may be secondary to tubercle, syphilis, chronic 
rheumatism, gout, traumatism, and lastly to scoliosis, when the 
ossification occurs in the concavity of the curve. Hereditary 
traumatic kyphosis is an example of general vertebral ankylosis 
and is probably due to ossification following injury to the anterior 
vertebral ligaments as a result of sudden straightening of the 
normal (or exaggerated) kyphotic curves. More common causes of 
general ankylosis are chronic rheumatism and spondylitis de¬ 
formans. These the writer considers essentially different from one 
another. In chronic rheumatism there is great enlargement of 
every part of the vertebrae, with irregular protuberances and osteo- 
phytic outgrowths and ossification of the intervertebral discs. In 
spondylitis deformans there is an osseous rarefaction, the ossifica¬ 
tion of the ligaments being compensatory, and there are no 
osteophytes formed; the bones of the pelvis are softened and the 
pelvis deformed. The former disease is inflammatory in origin, 
the first stage being a rheumatic arthritis: the latter consists in 
an ossification of the ligamentary structures to compensate for the 
softening of the vertebrae—a “ functional adaptation.” The con¬ 
sideration of these two conditions is entered into in great detaiL 
The paper is illustrated by photographs and drawings. 

Henry J. Dunbar. 


ON COMBINED PSYCHOSES. (Zur Lehre von den kombinierten 

(82) Psychosen.) E. Stransky (of Vienna), Allg. Ztschr.f. Psych., 
Bd. 63, H. 1. 

Since psychiatry has ceased to be satisfied with the description and 
analysis of symptomatological pictures, and has begun to group 
mental disorders according to the broader lines of their general 
development, clinical course, and symptomatology, combined 
psychoses have not been in favour. Cases may present symptom- 
complexes containing elements belonging to different mental 
disorders, but that does not justify the diagnosis of two indepen- 



dent and separate disease processes. It is true that a definite 
psychosis, with well-marked features, may develop in a person 
who has presented congenital anomalies of disposition; also a 
mental disorder may become complicated by the effect of various 
influences, alcohol poisoning, arterio-sclerotic degeneration, etc.; 
these latter are mere accessory additions. The possibility of the 
combination of an endogenous with an exogenous disease has been 
emphasised by some authors, but such combinations seem to be 
rare, e.g. the combination of manic-depressive insanity with general 
paralysis, or the combination of true paranoia with general paralysis. 
In such cases one has the right to talk of two psychoses. Other 
combinations are also possible— e.g. an amentia in the course of 
chronic paranoia, and the author gives the record of such a case. 
Besides the simultaneous combination, there may be the successive 
combination of two psychoses. The record is given of a patient 
with bad heredity who, after a first manic attack, recovered for two 
years, but later had a second typical manic attack, which, however, 
after a few months began to include extraneous elements ; patient 
now uttered confused delusions of a religious colouring, bad 
hallucinations of various senses, talked in a confused manner, 
producing more of a word-salad instead of the previous flight of 
ideas. A typical catatonic picture gradually developed, with 
alternation of excited and stuporous stages, with cataleptic 
phenomena, automatic response to commands, negativistic be¬ 
haviour, dilapidated and drivelling utterances, unmotived assaults. 
The patient has remained in the same condition for over a year. 

C. Macfie Campbell. 

(83) FABRICATION OF MEMORY). E. Angel (of Rochester), 
Joum. of Abnorrn. Psych., Oct. 1906. 

The casern one of a man 25 years old, who suddenly left his newly- 
married wife, and after about two weeks was discovered busily 
engaged canvassing in a town at some distance. The clue to his 
whereabouts was given by an absolutely false telegram which he 
himself had sent, dated from a non-existent hospital. When 
found, patient was in a peculiar condition similar to the hypnotic 
state. When examined by the author he gave three different 
accounts of his life. All of his accounts showed “subjective 
unconscious falsification of memory ” for the actual happenings 
of a somewhat uneventful existence. He filled the gaps with 
“visions and plausible impossibilities.” 

For example, in his first account, he referred in a most convinc¬ 
ing way to the death of his mother and his twin sister, the suicide 
of his father, his own training in King’s College, and his sub- 



sequent enlistment in the Canadian troops in the Boer War. All 
of these ideas were creations of an unstable imagination. 

In his second account he gave an equally false statement of 
his life, with an imaginative use of actual information with which 
he was confronted by a near relative; he is living the life of one 
Robbins, his name is no longer Rawlins, and the history which he 
first gave belongs not to himself, but to Robbins who is dead. 
According to his own account, he himself (Rawlins) and Robbins 
were associated as students in M‘Gill University, and as patients 
in a hospital in Winnipeg. Robbins died and left him (Rawlins) 
to suffer his sorrows, pay his bills, and inherit his estate. Facts 
show that Robbins is a myth, and that the patient was never 
a student at M'Gill University, nor a patient at Winnipeg. 

His third account is written after the “full recovery of his 
normal mentality.” He admits that his name is Rawlins and not 
Robbins, that his mother, brothers, and sisters still live, and that 
his father did not commit suicide, but died from natural causes. 
He still insists that he was a student at M'Gill University, but 
admits that from the time he entered the university up to the 
present time there have been periods of long duration for which 
he cannot account. Angel emphasises his belief in the honesty 
and frankness of the patient in giving these accounts, and declares 
that in such cases of so-called dual personality, much that has 
been accepted as actual occurrence during the dispossession of the 
ego could be proven to be an illusion, if the facts were sufficiently 
investigated. C. H. Holmes. 

(84) MENTAL DISORDERS. (Tiber Alkoholversuche bei Beur- 
teilung zweifelhafter Geisteszustftnde.) Tomaschny (of Trep- 
tow), Allg. Ztsrhr. f. Psych., Bd. 63, H. 5. 

The author recommends the experimental use of alcohol for 
diagnostic purposes, especially in certain medico-legal cases, where 
it is important to determine the responsibility of the individual 
and to ascertain whether he shows a pathological reaction to 
alcohol which may diminish his responsibility for acts committed. 
He records some interesting cases. The first patient had stolen a 
watch, and in prison had by his wild behaviour raised the sus¬ 
picion of simulation. After 14 days’ observation in the hospital, 
during which time he was irritable, inaccessible, and scolding, his 
mood suddenly changed, he became quite agreeable, claimed that 
he had an amnesia for the whole period, including the theft. 
After 5 weeks of total abstinence he was given a liberal dose of 
schnapps; about 36 hours later he had three epileptic attacks. The 
second patient had in a fit of irritation killed his child. During 



5 weeks’ observation he showed no striking peculiarity in behaviour; 
he was then given at lunch a bottle of beer and five small glasses 
of schnapps. When examined half an hour later he showed marked 
irritability and was extremely threatening. This condition lasted 
for a few hours. Five hours later he was again normal and 
denied any memory of having been irritable to the physician. 
Under the influence of alcohol his pupils became irregular. In 
another case the patient, who asserted that he was subject to 
epileptic attacks, and complained of numerous subjective com¬ 
plaints, said that he had had to give up a good position owing to 
epilepsy. An experimental dose of alcohol caused patient to cheer¬ 
fully narrate the truth about his past; he now boasted how much 
alcohol he could stand, while previously he had professed great 
intolerance towards alcohol. His pupils showed nothing abnormal, 
The author emphasises the importance of pupillary signs under the 
influence of alcohol as pointing to a pathological reaction. 

C. Macfie Campbell. 


Lektrire. Nervenleiden und Erziehung. Die ersten Zeichen der 
Nervosit&t des Kindeealters.) Prof. H. Oppenheim. Pp. 119. 
Berlin: S. Krager. Edinburgh: Otto Schulze & Co. 1907. 

The three lectures on “ Nervous Disease and Reading,” “ Nervous 
Affection and Education,” and “ The First Signs of the Neuroses in 
Childhood,” contained in Prof. Oppenheim’s small book, are ex¬ 
pressly prophylactic in aim; and though their author says perhaps 
too much in affirming that “ die Nervositat die Krankheit unserer 
Zeit ist ”—witness the extraordinary hysterical epidemics of the 
Middle Ages, and the fact that many of the lower races are singu¬ 
larly prone to hysteria—there can be no question that this branch 
of preventive medicine is one of pressing, and as certainly of 
increasing, importance. The first lecture treats of the influence of 
literature, and particularly of the daily press, on nervous subjects, 
and, whilst admitting the right of the public to a knowledge of 
scientific discoveries in the department of medicine, he inveighs 
strongly against the detailed publication in the daily journals of 
contributions to medical magazines, congresses, and the like, as 
fostering hypochondriacal fears, or, in the sexual sphere, exciting a 
prurient imagination, and urges his medical confreres to join in 
discouraging this tendency. Not only in ephemeral literature, 
but in modern poetry, the drama, belles-lettres, and particularly in 
novels, he finds a widespread, unhealthy appetite for the morbid 



and subtly indecent; pathological details, which might at one 
time have been given incidentally with blunt candour, now form¬ 
ing the sole motive of the book or play. In no wise con¬ 
cerned with public morality, but merely in so far as these 
tendencies find expression in the consulting-room, he finds here 
just grounds for their condemnation, and gives instances where 
neurasthenic and hysterical individuals have found here nurture 
for their complaints. The gist of the lectures is given in a 
quotation from Schopenhauer, “UmdasGute zu lesen, ist eine 
Bedingung, dass man das Schlechte nicht lese.” 

If it be true that medicine begins by being curative and ends 
in being preventive, it is essential that preventative measures 
should be instituted early in childhood, and should extend through 
what Dr Clouston in his “ Mental Hygiene ” calls the formative 
period of life. In his second lecture Prof. Oppenheim carefully 
considers the usual educational methods from the standpoint of 
the neurologist, and naturally finds considerable room for criticism. 
In particular the necessity for attention to the affective as well as 
to the purely intellectual side of development is emphasised—a 
point customarily disregarded by the pedagogue. Perhaps the 
most valuable part of this book is the third lecture, in which, out 
of his wide experience, the author describes the earliest symptoms 
of the neuroses in childhood (excluding organic brain diseases and 
the insanities), e.g. emotional reactions and their deviations from 
the normal in form and range, particularly the phobias and their 
motor expression, the liability to hallucinatory delirium, the ten¬ 
dency to imaginative lying, the so-named pseudologia phantastica, 
the disorders of sleep, the tics, and many habitual motor 

Incidentally, Prof. Oppenheim states that he has been struck 
by the extraordinary liability of the offspring of mixed marriages, 
particularly between Jews and Christians, to nervous affections. 
This seems a point of some importance, and it is unfortunate that 
Prof. Oppenheim is unable to give his opinion statistical support. 1 




Dr RenE Charpentier. Pp. 227. Paris: G. Steinhefl. 

Edinburgh : Otto Schulze & Co. 1906. 

Throughout the ages, poison has been a favourite weapon of 
women, whether the object has been to pursue intrigues, to gratify 

1 Prof. Karl Pearson, in reply to an enquiry from the reviewer, states that he 
lias no data on this point, and suggests that medical men in India might give 
mueh information as to Eurasians, whilst in certain districts in London the results 
of marriages between English and German and English and Jews might be observed* 



feelings of revenge or jealousy, or merely in obedience to deep- 
se&ted pathological impulses. The women who have become 
notorious in history for the crime of poisoning have often been 
found possessed of a peculiar mentality. It is only within the last 
century that the records of the investigations of such crimes have 
contained the report of a thorough medical examination of the 
author of the crime with a view to determine responsibility. The 
cases on record form a good starting-point for the analysis of the 
mental constitution and idiosyncrasies of this group of criminals; 
while a historical review shows many analogous cases, where, how¬ 
ever, the mental diagnosis must be retrospective. The author of 
this study of female poisoners runs over the names famous in 
history from this point of view, and precedes his historical review 
with examples from classical mythology. The crimes of ancient 
Greece and Rome are shortly referred to; in Rome especially there 
were such epidemics of poisoning that special laws were made to 
meet the danger. No poisoners are better known, perhaps, than 
the infamous Borgias, but the author quotes the passage where 
Gregorovius defends Lucretia Borgia, attributing her crimes to her 
unfortunate environment. A special chapter is devoted to the 
notorious Marquise de Brinvilliers, who combined a profound skill 
in simulation with a moral anaesthesia. On a par with her crimes 
were those of the hysterical Madame de Montespan. 

After finishing the historical account, Charpentier takes up the 
clinical analysis of this group of hysterical degenerates ; he endea¬ 
vours to separate the hysterical incidents from the stigmata of the 
degenerate constitution ; from the latter point of view these persons 
show kinship with the moral imbecile. Their hysterical mentality 
is shown by their suggestibility and their well-marked tendency to 
mental dissociation. The intellect of the cases discussed showed 
at the same time evidence of considerable brightness and lapses 
leading to coarse blunders. Aboulia coexisted with obstinacy, 
and affective anaesthesia with an excessive susceptibility to 

In the third division of the book, the author discusses the 
medico-legal questions which such cases raise. These unfortunate 
people are suited neither for the prison nor for the hospital for 
the insane ; they are abnormal beings, who for their own sake and 
for the sake of society should be detained in special asylums, and 
the conditions under which a return to social life might be allowed 
could be determined by the physician in charge, under the autho¬ 
rity of the courts. 

The book is written in an agreeable style, contains some in¬ 
teresting illustrations, and presents in language not too technical 
a subject which is of considerable social and medical interest, 

0. Macfie Campbell. 





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systems. I). Ztschr. f. Nercenheilk., Bd. 31, H. 5-6, 1906, 8. 885. 

ARTURO MORSELLI. L© lesioni nerroee dei feti n&ti da madre tubercolosa. 
Rie. di Patol. nerv. e ment., Vol. xi, f. 11, 1906, p. 541. 

WILFRED HARRIS. The Nervous System in Influenza. Practitioner, Jan. 
1907, p. 70. 


BERNHARDT. Zur Kenntnis der sogen. angeborenen MuskelschlafFheit, 
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1907, S. 2. 


HUET. Neuritis, verursacht durch Crcosotum phosphoricum. Neurol. Cenhnlbl 
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J. H. LLOYD. Paralysis of the Peroneal Nerve following Child-birth. N. V. 
Med. Jour a., Dec. 2*2, p. 1209. 

WAN DEL. Uber Stbrungen im Gebiete des Nervus medianus. />. Ztschr. /. 
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J. N. HALL and S. D. HOPKINS. Landry's Paralysis, with Report of Five 
Cases. Joum. oj Am. Med. Ass., Jan. 12, p. J04. 

CURTIS WEBB. A Suggestion for the Treatment of Cases of Chronic Sciatica 
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A. S. TAYLOR. Results from the Surgical Treatment of Brachial Birth Palsy. 
Joum. of Am. Med. -4m., Jan. 12, p. 96. 


Tab?*.—CAM US et SEZARY. Tabes cervical avec Ataxie unilateral©. (Soc. de 
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RAYMOND et HUET. Tabes probable avec Atrophic des muscles de la nuque, 
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LORTAT-JACOB. Hyperesth6rie tactile douloureuse h Topographie Radiculaire 
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Disseminated Sclerosis.— MENNELL. Notes on a Case of Disseminated Sclerosis. 
Lancet, Jan. 19, 1907, p. 160. 

Combined Sclerosis.—PIERRE MARIE. Forme s£nile de Sclerose Combine©. 

(Soc. de Neurol.) Rev. Neurol., d£c. 30, 1906, p. 1188. 

Frmctnre Dislocation. — MtJLLER und LERCHENTHAL. Zwei F&lle von 
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1906, S. 398. 

Tsnonr.-BATTEN. A Lecture on the Diagnosis of Tumours of the Spinal Cord. 
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Spinal Caries. —ALQU1ER et LHERMITTE. Mai de Pott et syringomy61ie. Rev. 
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Meningitis. —T. MORRELL and H. E. WOLF. Cases of Meningitis with Isolation 
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L. JEHLE. Ueber das Vorkommen des Meningokokkus und des Micrococcus 
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SHOLTO DOUGLAS. A Case of Influenzal Meningitis. Lancet, Jan. 12, 

1907, p. 86. 

Arterfto-gelerosls.—JOSEPH COLLINS. A Definite Clinical Variety of Cerebral 
Arterio-scleroeis. Joum. of Nerv. and Ment. Die., Dec. 1906, p. 750. 



< leMlpleflt.—MIRALLlfe et GENDRON. L’6tat dee muscles masticateurs dans 
, rh£mipl£gie. Rev. Neurol., d£c. 30, 1906, p. 1145. 

Bulbar Paralysis*—GRENET at TANON. Syndrome Bulbaire (Lesion rachi- 
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BAB1NSKI. Lesion Bulbaire unilat^rale : Therm o-asy metric et Vaso-agym6trie ; 
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die. 30, 190J, p. 1177. 

EDUARD MULLER. Tiber ein eigenartiges, scheinbar typisches Symptomenbild 
beiapoplektiformer Bulbarlahmung (nebat Bemerkungen iiber perverse Tempera- 
turempfindungen und bulbare Sympathicusparesen. D. Ztsckr. f. NervenkeUk ., 
Bd. 31, H. 5-6, 1906, S. 452. 

Tauonr.—B. SACHS. Some Notes on the Diagnosis and the Result of Suigical 
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SOUQUES. Tumour Cercbrale de la region des circonvolutions pariltalec 
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VINCENT. Ndoplasme intracranien, Troubles Bulbo-protublrantiels, H£mi- 
asynergie. (Soc. de Neurol.) Rev. Neurol., dec. 30, 1906, p. 1196. 
Echinococcus.—OSVALDO FEDERICI. Un caso di cisti da echinoooooo del 
ventricolo laterale con sindrome prevalentemente cerebellare in'un bambino, Riv. 
de Patol. nerr. e merit, Vol. xi., i. 11, 1906, p. 505. 

Abscess.—VOSS. Vier Todesfalle in Folge von Hirnabszess nach otitischer Sinus 
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ftlnns Phlebitis.—ST CLAIR THOMSON. Cerebral and Ophthalmic Complica¬ 
tions in Sphenoidal Sinusitis. Tran*. Med. &oc. of Ix>nd., Vol. xxix., 1906. 
Cerebral Diplegia.—A. M. FORBES. A Study of the so-called Infantile Paralyses. 
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W. J. BUTLER. Etiology of Cerebral Palsies in Children. Joum. of Am. Med. 
An., Dec. 29, p. 2139. 

BAUDON. Le Syndrome de Little. Valeur nosologique, etc. (Thise.) Bousset, 
Paris, 1906. 

General Paralysis*—LEBRET. Paralysis g6n6rale et Psychosee dans la syphilis 

acquire. Rnusaet, Paris, 1906. 

AUGUST HOCH. A Report of Two Cases of General Paralysis with Focal 
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J. W. FISHER. Two Cases of Dementia Paralytica—one associated with a large 
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Jan. 5, p. 5. 


CHOTZEN. Casuistischer Beit rag zur Frage der chronischen Alkoholhalluzinosis. 
Cenlralbl. f. NervenkeUk. u. Psyckiat., Jan 1, 1907, S. 1. 

CASEY A. WOOD. Some Recent Cases of Death and Blindness from Wood- 
alcohol Poisoning. Bril. Med. Joum., Dec. 29, 1906, p. 1855. 


FIN CKH. Zur Frage der Intelligenzpriif ung. CerUralbLf. NervenkeUk. u. Psyckiat., 
Des. 15, 1906, a 945. 

BADGER. Die Bedeutung der psychoanalytischen Methode nach Freud. 
Cenlralbl. f. NervenkeUk. u. Psyckiat ., Jan. 15, 1907, S. 41. 

C. W. BURR. Trauma of the Head as a Cause of Insanity. Joum. of Am. Med. 
Ass., Jan. 5, p. 33. 

F. CHOTZEN. Ein Beitrag zur Atiologie der Amentia. Allg. Zeit. f. Psyckiat 
Bd. 63, H. 6 p. 786. 

HAM PE. Uber den Sohwacbsinn, nebst seinen Beriehungen zur Psychologic der 
Aussage. Vieweg A Sohn, Braunschweig, 1906, M. 2. 

JUNG. Uber die Pbychologie der Dementia praeoox. Marhold, Halle, 1907. 
M. 2.50. 

J. FINCKH. Uber Hitzepsychosen. Allg. Zeit. f. Psyckiat., Bd. 63, H. 6, 
p. 804. 

A. GORDON. Migrainio Psychoses. Joum. of Am. Med. Assoc. Jan. 5, 
p. 38. 

T. CLAYE SHAW. The Psychoses of Influenza. Practitioner , Jan. 1907, p. 86. 
GIMBERT. Contribution a l’6tude des psychon^vroses ches les tuberouleux. 
(Thhe.) Durand, Chartres, 1906. 

ROUGlS. De bali6nation mentale consecutive k la fikvre typhoid©. Ann. mid.- 
psychol., jan.-f^v. 1907, p. 5. 

SIERAU. Zur Frage des myxbdematbsen Irreseins. Voss, Hamburg, 1906, 
M. 1. 



SERGE SOUKHANOFF. Contribution h T6tude de la psychos© de Korsakoff k 
marche continue. Ann . mSd.-ptychol., jan.-f6v. 1907, p. 49. 

A. GREGOR. Beitrage zur Kenntnis der GedSchtnisstbrung bei der Korsa- 
kotTschen Psychose. Monatssckr. f. Psychiat. n. Neurol Jan., p. 19. 

A. HEGAR. Tjber Arbeitsentlohnung~ in unseren Irrenstalten. AUg. Zeit. f. 
Psychiat. y Bd. 63, H. 6, p. 825. 

trique de Munich. Ann. mid.-psychol. , jan.-f6v. 1907, p. 58. 


Kpllcpij.—-W. ALEXANDER. Scientific and Clinical Reports on Epilepsy. 
Liverpool Aftdico-Ch i rurgical Journal, Jan. 1907, p. 167. 

J. M'lLRAITH. The Etiology of Convulsions in Infancy and Childhood. Med . 
Chronicle , Jan. 1907, p. 223 (concluded). 

PELZ. Ein Fall von genuiner Epilepsie mit darauffolgender Dementia paralytica. 
Neurol. CentraIbl ., Jan. 2, 1907, S. 14. 

HEILBRONNER. Uber gebiiufte kleine Anfalle. D. Ztschr . /. Nervenheilk.. 
Bd. 31, H. 5-6, 1906, S. 472. 

LEON LORTAT-JACOB. A propos du regime dechlorur^. dans l’gpilepsie de 
Tenfant hyperch!orurie d alarme pr6c6dant une congestion pulmonaire. Rev. de 
Med., Jan. 10. 

A. PELZ. Ueber periodische transitorische Bewusstseinsstbrungen nach Trauma. 
MonaUschr. f. Psych tat. u. Neurol. , Jan., p. 53. 

BENNION. Some Observations on the Treatment of Epilepsy in the Insane with 
Strontium Bromide. Lancet , Jan. 5, 1907, p. 19. 

Chorea.—LARRAZET. De la choice rgeiaivante chez l’enfant ( Roy, 

Lyon, 1906, fr. 1.25. 

Hysteria.—BABJNSKI. Ma conception de ThystArie et de l'hypnotisme. Durand, 
Chartres. 1906. 

PAULSOLLIER. La definition et la nature de Thyst^rie. Arch. gin. demSd. y 
oct. 9, 1906. p. 2585. 

OSKAR FISCHER. Ein weiterer Beitrag zur Klinik und Pathogenese der 
hysterischen Dysmegalopsie. Monatsschr. f. PsychiaX. ti. Neurol Jan., p. 1. 
Neurasthenia.—PASCAL. Pseudo-neurasthenia prodromique de la d6mence 
pr£coce. Preset mid., Jan. 19, p. 42. 

MONTHELIE. La N6vrose traumatique et la loi sur les accidents du travail. 
(These.) Rousset, Paris, 1906. 

Scleroderma.—NIXON. Scleroderma and Myositis. Lancet, Jan. 12, 1907. p. 79. 
Sleeping Sickness.—MARTINI. Trypanosomenkrankhoiten (Schlafkrankheit und 
Kala-azar). Fischer, Jena, 1907, M. 2. 

Exophthalmic Goitre.—MOSSE. Zur Kenntnis einigerseltener Storungen bei der 
Basedow’schen Krankheit. Berlin, klin. Woch., Jan. 7, p. 14. 

Adlposa Dolorosa.—SEZARY. Quatre cas d’adiposa aouloureuse, maladie de 
Dercum. Rev. de Mid.. Jan. 10. 

Myasthenia Gravis.—SITSEN. Myasthenia gravis. Berlin . klin. I Voch., Dec. 31, 
p. 1669. 


O. ROSSI. La funzione corticale della visione. Tipografia Cooperativa, Pavia, 

COLIN K. RUSSEL. The Vision Fields in Cases of Indirect or Incomplete 
Lesions of the Optic System. Journ. Nerv. and Merit . Die., Dec. 1906, p. 760. 

A. P1LCZ. Zur prognoetischen Bedeutung dee Argyll - Robertson schen 
Phanoraens. MonaUschr. f. PsychiaX. u. NeuroL, Jan., p. 46. 

REICHARDT. Ueber willkurliche Erweiterung der Pupillen. Deutsch . mtd. 
Woch ., Jan. 24, p. 142. 

HERMAN KNAPP. Dependence of Accommodation and Motility on the Refrac¬ 
tion of the Eye. Brit. Med. Journ., Dec. 29, 1906, p. 1867. 

FERNAND LEVY. Svndrome Gass6rien dfl k une N6vrit© sclerogommeuse des 
trois branches du Trijuneau. (Soc. de Neurol.) Rev. Neurol. , d6c. 30, 1906, 
p. 1194. 

HEYRAUD. De la paralysie du moteur oculaire extern© d’origin© otitique. 
( This*.) Rey et Cie., Lyon, 1906, 8 fr. 

ALFRED GORDON. The Pathogenesis of Facial Hemiatrophy. N. Y. Med. 
J ourn. , Jan. 12, p. 56. 

WITTMAACK Weitere Beitrag© zur Kenntnis der degenerativen Neuritis und 
Atrophi© des HOmerven. Zeit. f. Ohrenheilk ., Bd. 53, H. 1, p. 1. 




O. HILDEBRAND, F. MttLLER, u. F. v. WINCKEL. Das ‘Mntermittierende 
Hinkon” als Vorstufe der spontanea Gangr&n. Sammluno khnuchei' Vo/i'trOge. 
Nr. 439. 

H. BENEDICT. Ueber metamore Sensibilitatsstdrungen bei Gehimerkrankungen. 
Wien. iclin. Woch., Jan. 17, p. 66. 

LONG et ROUSSY. Hdmi&nesthesie Cer6brale par lesion de la Couche Optique 
et de la Calotte p6donculaire, sans participation du segment post^rieur de la 
capsule interne. (Soc. de Neurol.) Rer. Neurol ., d4c. 30, 1906, p. 1202. 

CAMUS et S1&ZARY. Un cas de Radiculite sensitivo- mo trice. (Soc. de n£urol.) 
Rev. Neurol ., dec. 30, 1906, p. 1172. 

GRENET et TANON. Arthropathies nerveuses, Aggravation des lesions et 
amelioration fonctionnelle. (Soc. de Neurol.) Rer. Neurol ., dec. 30, 1906, 
p. 1192. 

HIGIER. Schweissanomalien bei Rlickenmarkskrankheiten. Neurol. Centralhl. 
Jan. 2, 1907, S. 19. 

PAUL COURBON. Automatisme ambulatoire (observations cliniques). A nn. 
mid.‘psychol. % jan.-fcv. 1907, P. 22. 

NOIuA. Sur les rapports des reflexes cutanea avec la sensibilitc. Journ. de 
Neurol ., dec 20, 1906, p. 609. 

KUTNER. Uober des Verhalten einiger Reflexe im Sclilaf. Dei fitch, med. IIV//., 
Jan. 17, p. 98. 

TRENDELENBURG. Beobachtungen liber Reflexe und Tonus an den hinteren 
Extremitiiten. Archie, f. Anal. u. Physiol ., 1906, p. 2131. 

LEVENSOHN. Kuree Notiz zur Kenntnis der Lidreflexe. Klin. MomUdd. f. 
Augenheill 1907, p. 56. 

CHARPENTIER. Signe de Babinski dans la Choree de Sydenham. (Soc. de 
Neurol.) Rer. Neurol ., dec. 30, 1906, p. 1176. 

PIERRE MARIE on Aphasia. Leading Article. Brit. Med. Jonrn Dec. 
29, 1906, p. 1879. 

P. MARIE. Rectifications ^ propos de la question de 1’aphasie. Preste w£d. w 
Jan. 12, p. 25. 

F. X. DERCUM. Mario’s Views on Aphasia. N. Y. Med. Journ ., Jan. 5, p. 7. 
LADARNE. Aphasie et Anarthrie. Presae m&d., dec. 22, p. 826. 

V. VLEUTERN. Transitorische Aphasie bei Alkoholdelirien. Ally. Zeit. J. 
Psychiat , Bd. 63, H. 6, p. 767. 

HARTMANN. Beitrage zur Apraxielehre. Karger, Berlin, 1906, M. 2. 
VANDER VLOET. Apraxie et d6mence. (Suite.) Journ. de Neurol., dec. 20, 
1906, p. 614. 


LAUNOIS et POROT. Lex nouveaux traitements dans les maladies nerveuses. 
Baillikre et fils, Paris, 1907, fr. 1.50. 

LUTTENBECHER. Nervenleiden, ihre Heilung durch psychiscbe und physische 
Behandlung. Elischer Nachf., Leipzig, 1907, M. 1.50. „ 

OUDIN. fetat actuel de la radiumth6rapie. Ann. <T Eleclrobiol. , nov. 1906, 
p. 772. 

BILLINKIN. A propos de Telectrisation dans les nSvralgies et dans l’obesit£. 
Bull . de la &or. Franchise d' Electrothtr., jan. 1907, p. 15. 

KILIANI. Schldsser’s Treatment for Trigeminal Neuralgia. Med. Rec. t Dec. 
29, p. 1019. 

BILLINKIN. Nevralgie du Trijumeau. Gu6rison par T61ectricit6. Bull, d la- 
Soc. Francaise (VElectrotUr., d£c., 1906, p. 249. 

LOWENTHAL und WIEBRECHT. Uber Behandlung der Tetanic mittelst 
Nebenschilddriisenpraparaten. D. Zttchr. f. Nervenheilk ., Bd. 31, H. 5-6.1906, 
S. 415. 

G. HUDSON-MAKUEN. The Physiology of Language and its relation to the 
treatment of Stammering. N.Y. Med. Journ. , Dec. 29, p. 1261. 

C. E. ATWOOD. A neurological critique of recent Surgical Treatment of cere¬ 
bral Birth Palsies. N.Y. Med. Journ., Jan. 19, p. 107. 

CHARLES PHELPS. The question of Early Operation in cases of Intracranial 
Injury. AnnaD of Surgery, Dec., p. 801. 

BASIL KILVINGTON. The Treatment of Paralytic Talipes Valgus by Tendon 
Transplantation. Brit. Med. Journ., Jan. 19, 1907, p. 134. 

* A number of references to papers on Treatment are Included in the Bibliography under the 
individual Diseases. 



fleurolOQE anb ps^cbiatr^ 

©riginal Reticles 



Labyrinthine deafness is not rare in those who suffer from 
tabes, but seldom can be ascribed, with any confidence, to 
atrophy of the auditory nerve, analogous to that which is so 
common in the optic nerve. It may be suspected when the 
deafness is bilateral and progressive, but these features do not 
justify more than a suspicion. Two characters, however, make 
the diagnosis probable. These are: (1) a progressive reduction 
of hearing from above and below, analogous to concentric 
restriction of the fields of vision ; (2) a loss in the centre of the 
range, analogous to a central scotoma in vision. Both are rare. 
Their significance is especially great if the deafness accompanies 
optic nerve atrophy. This indicates that the morbid influence 
which induces tabes is of a character to affect the nerves of 
special sense, especially the optic nerve, in greater degree than 
the sensory nerves of the muscle. 

It is a matter of common observation that in tabes, if the 
optic nerves suffer, the legs often escape, and vice versa. It was 
said by Benedikt that the relation is one of cause and effect, 
that the affection of one saves the other from suffering. This 
has indeed been called “ Benedikt’s law.” I think, as I pointed 
out many years ago, that the true explanation is a difference in 
the cause. If we assume that this is a post-syphilitic toxine, 
B. OF N. & P. VOL. V. NO. 3— M 



as is probable, the marked difference in the degree of the various 
symptoms of tabes can only be explained by differences in the 
character of the toxine. Thus only can we understand the fact 
that one patieDt may suffer intensely from pains, another hardly 
at all; that in one laryngeal and gastric crises may be frequent, 
and in another never occur. The difference in the toxine may 
be ultra-minute, and yet adequate to act chiefly on nerve 
structures that differ in susceptibility in corresponding degree. 
Thus the inverse relation between the affection of the eyes and 
of the limbs is not a direct connection, as Benedikt supposed, but 
an indirect consequence of the nature of their cause. This view 
is confirmed by the fact that exceptions are not rare. The optic 
nerves may suffer when there is extreme ataxy. 

I. Bi-terminal Reduction of Hearing , x analogous to concentric 
restriction 3 of the field of vision. In one case of this kind the 
patient, when first seen, could hear no note above E 1 (660 vibra¬ 
tions) 8 or below G! (198 vibrations). A few months later the 
range of hearing had become still further reduced, but from below, 
not from above ; hearing was limited by E (330) and E 1 (660), 
the two E notes within the treble. Even E flat was inaudible. 
A few months later even this octave had disappeared and he was 
totally deaf on that side. 

II. Auditory Scotoma .—A loss in the middle of the range of 
hearing, analogous to a scotoma in the middle of the field of 
vision, is also, possibly, evidence of primary atrophy of the nerve. 
It is rare, and its significance may not be beyond question. The 
following case is therefore important, because other facts support 
the assumption of primary atrophy. I will mention very briefly 
the chief symptoms. 

The patient was first seen in 1899, when 57. There was a 
strong suspicion of syphilis at 19. The right knee-jerk was 
absent, the left fair. Sensibility to pain was defective on this 
leg and on the right side of the abdomen; it was almost lost on 

1 “ Bi-terminal” seems the only fit adjective for “at both ends.” 

* The word so often employed, “concentrio limitation of the field,” is undesir¬ 
able, because a field without limit must be very rare indeed. 

* This rotation is that which I urged, as most convenient and least liable to 
error, in this Review for April 1908. In it the unnumbered C is the middle C, i.e. 
that between the treble and the bass (256 vibrations); C 1 and C x are respectively in 
the second space from the top of the treble and from the bottom of the bass staves. 
The number of vibrations is easily ascertained by remembering that Cs=38 ; there* 
fore Ca=66, Ci = 182, C=264, etc. 


the thigh. Tactile sensibility was normal There was very 
slight dystasia (Rombergism). Micturition was tardy; sexual 
power lost. The pupils were small, inactive to light, acting 
with accommodation. His optic discs were pale, the right more 
than the left. Vision, corrected for presbyopia, right t; left 
quite good. Fields normal. A central scotoma, relative, was 
found in the right eye, larger for red. 

It is needless to follow the case in detail. The tabetic 
symptoms have scarcely increased. Indeed, the only change is 
that the left knee-jerk after a time could only be obtained with 
reinforcement, and is now lost. Vision lessened a little during 
the first year; the right scotoma became absolute, irregular in 
form, extending to about 10°, and the field lessened above and 
outwards. In the left eye, central dimness developed, with a 
larger loss for red around it. Then his vision became stationary 
for about three years. During the last three years it has failed 
steadily, and during the last six months rapidly. The peripheral 
restriction of the right field steadily increased, and vision 
became dim in the part between it and the scotoma, so that 
three months ago he could barely see light with this eye. The 
scotoma in the left became absolute, but beyond it he could 
make out A. Since then, peripheral vision has rapidly passed 
away in this eye also, and now he can only discern light from 
darkness. His optic discs have long presented the appearance 
of advanced atrophy. I have given these details on account of 
the greater affection of the right side in both legs and eyes, and 
of the failure of sight by a central loss. I should add that he 
had always been a very small smoker. 

During the last year he has noticed that his hearing was not 
so good as formerly, especially for the high-pitched voices of 
children. On testing his hearing it was found to have a range 
unusually high for his age (now 65). He could hear Galton’s 
whistle (the high whistle-sound being carefully distinguished 
from the sound of blowing) with each ear up to 12,000 vibra¬ 
tions. With the right ear, on passing downwards, he could hear 
each sound to 7000 vibrations, but no lower note. He could 
not hear the C 8 tuning-fork (2112), but could the C 2 (1056) 
and all lower notes, through the bone as well as through the air. 
C* was not heard even through the bone. On the left side there 
was a similar loss, but less extensive. He could hear C 2 , but not 


C 8 , but the loss only extended to 5000 vibrations, which he could 
hear, and higher notes up to 12,000. On this side also the 
result was the same through the air and the bone. 

The association of this auditory loss with the central scotoma 
by which sight failed, first and chiefly, is remarkable. It 
constitutes strong evidence that the auditory scotoma was 
the result of commencing primary atrophy of the nerve. At 
the same time the subject is a difficult one. In this case 
the loss was at the region of the highest tuning-fork available, 
probably about two octaves. This region of the range of hearing 
is not comparable to the central region of the field of vision 
occupied by the visual scotoma. There is no special functional 
capacity at that part of the range of hearing as there is in the 
field of vision. But failure of central vision in this manner is not 
common in tabes. More frequently there is a progressive re¬ 
striction of the field, with general failure. The morbid changes 
in tabetic atrophy with a central scotoma have not, I think, 
been ascertained. It may be that they are independent of 
function, and of a character that the auditory nerve may also 
undergo. Thus the apparent correspondence in the visual and 
auditory failure may be more than apparent, and the seeming 
significance of the auditory scotoma may be real. 


By C. W. CHAPIN, M.D., 

Junior Physician, Manhattan State Hospital, Ward’s Island, N.Y. 

This study was prompted by the difficulty encountered in the 
analysis of atypical psychoses, in which alcohol has played a 
prominent part. We observe every possible symptom-complex 
as an apparently more or less direct result of alcoholic excess ; 
in many cases this excess is the first symptom of the psychosis, 
and not its cause; the exact facts as to the patient’s habits are 
often not obtainable ; it thus becomes important to know what 
conclusions we are justified in drawing from the clinical picture 

1 Read at a Conference of State Hospital Physicians at Manhattan State Hospital, 
Ward’s Island, N.Y.C., December 12, 1906. 



itself, as to the part alcohol has played in the etiology. An 
attempt is made in this study to gain a bird’s-eye view of the 
group as a whole, and to trace through the maze of divers? 
symptoms and sub-groups some common element to assist us in 
sizing up doubtful cases. 

Speaking of acute alcoholic intoxication, Kraepelin says: 
“ The effect of alcoholic poisoning upon the mind, in so far as 
it is known, consists essentially in the impairment of the grasp, 
retention, and elaboration of external impressions, and in facilitat¬ 
ing the release of the impulses of the will ... as all good 
observers agree, even very small quantities of alcohol materially 
impair the efficiency for high-grade mental effort. A person is 
less able to collect his thoughts and to follow an involved sequence 
of ideas. With further poisoning the impairment of grasp and 
reason becomes still more pronounced. The individual no 
longer rightly understands what is said to him and what goes 
on about him, cannot apply his attention nor follow a train of 
thought ... as the loss of grasp and reason progresses, he 
becomes insensitive, irrational, and finally completely uncon¬ 
scious. . . . The psychomotor irritative symptoms keep pace 
with the intellectual disturbance. They begin with a mild 
exhilaration, which is felt after the ingestion of even small doses 
of alcohol, with the loss of the delicate inhibition which regulates 
with accuracy his daily conduct and manner. He becomes care¬ 
free, is in good spirits, cheerful, unrestrained in speech and 
action, courageous, even reckless. On account of the facility 
of the release of motor impulses, his strength and capacity for 
work seem to be increased in contrast with their actual material 
diminution. From this arises the unfortunate, widely diffused, 
but entirely erroneous impression that alcohol is a stimulant. . . . 

“ In the affective field the first stage of intoxication is mani¬ 
fested by a distinct well-being and happy, cheerful humour. The 
cares and vexations of daily life recede into the background. A 
person becomes trifling, more accessible and amiable. Meanwhile 
irritability becomes manifest; he is provoked to abrupt changes 
of mood, is overbearing, gives himself up to outbreaks of temper 
and to fits of passion with grave excesses.” 

After the numbing effect of alcohol upon the sensorium has 
worn off, another affect makes itself felt. This consists in rest¬ 
lessness, the feeling that something is wrong, the sense of psychic 



distress familiar to a large percentage of adults from their experi¬ 
ences next morning. It is difficult to find any one word to cover 
all the various manifestations of this feeling, but for want of a 
better term we may speak of it as apprehensiveness. 

The primary and most fundamental symptoms of acute intoxi¬ 
cation thus seem to be early psycho-sensory anaesthesia, and later 

In the anomalous forms of intoxication we find usually a 
severe grade of disturbance of consciousness, usually accompanied 
with excitement, impulsiveness, and often criminal tendencies, 
but without serious paralytic effects. There may also be present 
distinct hallucinations and conditions of keen anxiety, which are 
otherwise foreign to intoxication. The two fundamental disturb¬ 
ances mentioned above explain for the most part the features 
of this group also, but in addition we have to reckon with a 
morbid predisposition which adds to the picture certain features 
of its own. * 

The restlessness, apprehensiveness, and irritability of the 
*' sobering off” period are by no means the only manifestations 
of the painful affect. In certain cases we find, following severe 
or prolonged alcoholic excess, an outburst of terrifying hallucina¬ 
tions with corresponding delusions, the acute hallucinatory form 
of alcoholic psychosis. In these cases the orientation is usually 
retained, the morbid ideas and experiences are within the range 
of possibility, and do not come into any glaring contradiction with 
the actual situation. This requires but a brief mention, being a 
very pure form of psychosis, characterised by symptoms condi¬ 
tioned by the apprehensive state of the patient 

Chronic alcoholism is not regarded by the community at 
large as a psychosis, but the chronic alcoholic exhibits many 
psychopathic features. A mild psycho-sensory defect with eu¬ 
phoria determines the carelessness, improvidence, disregard of 
the requirements of morality and convention, the droll humour, 
over-valuation of self, and uncouth and overbearing manner. 
The apprehensive features commonly displayed are irritability, 
querulousness, jealousy, and suspicion. The alcohol, however, 
should not be blamed for all the manifestations of original 

Of alcoholic stupor, Wernicke says: “The clouding of the 
sensorium in these cases, the somnolence, which is only paralleled 



in cases of brain-tumour, may persist for weeks and even months, 
and makes the picture so similar to that of organic brain disease 
that for my part I have no doubt of the organic basis in hydro¬ 
cephalus intern us. Further, the disturbance of gait manifested 
by the patients as soon as they are out of bed resembles only 
that of senile hydrocephalus internus. The pulse too may 
be somewhat slowed, and general muscular rigidity with very 
distinct exaggeration of mechanical irritability is likewise common 
to these cases and to cases of senile hydrocephalus internus.” 

A few other forms of alcoholic psychosis require but a brief 
mention. Alcoholic paranoic conditions are gradually developed 
from long-continued intemperance, or may remain as the residual 
of otherwise recovered acute forma The worst periodical 
drinkers show in many cases characteristic ear-marks of some 
constitutional tendency, either of the epileptic, hysterical, or 
manic-depressive type. Alcoholic pseudo-paralysis is charac¬ 
terised by deterioration, particularly in the field of memory and 
grasp, and by the prominence of physical signs. Alcoholic 
deteriorations will be discussed later. 

In the polyneuritic psychosis (Korsakoff's psychosis) we find 
again, particularly at the beginning of the disorder, apprehensive 
symptoms in the way of restlessness, irritability, querulousness, 
sometimes a persecutory delusional trend and depressive hallucina¬ 
tions. But the feature which distinguishes this group is the 
defect in grasp of a special type, accompanied by euphoria. 
This defect is an impairment of retention, or rather of the ability 
to impress passing experiences upon the memory. Here again 
we find a familiar phenomenon. Though the psycho-sensory 
defect and euphoria are not identical with that of the first stage 
of intoxication, yet the analogy has led certain writers to suggest 
the inference that the defect in grasp is the direct result of the 
toxic action of the alcohol, while the apprehensive features are 
the result of poisons, elaborated in the course of disordered 
digestion and due to perverted metabolism. With the memory 
defect there exists in a certain percentage of cases a tendency to 
fabrication, analogous to that found in other similar conditions, 
for example, in senile psychoses. The loss of the connecting 
links with the past may render a correct time and place orienta¬ 
tion impossible ; but the patient grasps his immediate surround¬ 
ings and reacts in a fairly normal manner thereto. In many 



cases, however, the hold even on the immediate environment is a 
precarious one, and is entirely lost for short periods of time, 
during which the patient not only fills in the narrative of his 
immediate past with fabrications, but distorts his immediate 
impression, mistakes the place for some familiar locality, and, 
assisted by illusions and hallucinations, proceeds to engage in his 
accustomed business, or becomes the victim of imaginary fantastic 
experiences. In other words, we have temporary episodes of 

The boundary line between these two conditions of poly¬ 
neuritic psychosis and delirium is not a sharp one. For instance, 
one of our patients, though in general a fairly typical case of 
polyneuritic psychosis, yet persisted in believing that her child 
was somewhere about the place, saw it at times in the next bed, 
saw her mother among the patients in the yard, and had several 
episodes of a few seconds’ duration, evidently provoked by neuritic 
pain and cardiac disturbance; during these she would manifest 
great anxiety, clasp her arms over her breast, believing herself to 
be holding her child, and seize the examiner’s hand, calling him 
by the name of her husband. These states, which are really 
episodes of delirium tremens, are common enough in this 
psychosis, and show the close analogy of the two conditions. 

In delirium tremens the defect in grasp is manifested by a 
failure of retention, the distortion of immediate impressions, and 
replacement of reality by fabrications, hallucinations, occupations, 
and imaginary fantastic experiences, due largely to the fact that 
the products of a lively imagination have come to have more 
reality to the patient than the testimony of the clouded sensorium. 
The apprehensive feature is seen in the colouring of most of the 
patient’s experiences by anxiety and fear; for instance, the 
driver in his delirium makes desperate efforts to back his team 
out of all sorts of imaginary difficulties and dangers. Many of 
the hallucinations are also of a most terrifying content. 

A characteristic feature is a certain grim humour, the Galgen- 
humor (gallows-humour) of the Germans. The patient, though 
perspiring with anxiety, views the situation in a facetious light, 
offers droll comments, and pictures in a joking way his hallucina¬ 
tions. Cheerfulness and deathly terror follow close upon each 
other. Bonhoffer regards the euphoria of the delirious patient 
as a sign of mental weakness. Kraepelin, however, takes another 



view : “ I have not been able to convince myself that it is con¬ 
fined to cases of psychic enfeeblement, and much prefer to ascribe 
it to the happy, care-free state which we observe in alcoholics 
generally, and in Korsakoff’s psychosis especially, and which is 
also characteristic of simple intoxication." 

It may be urged that delirium tremens is not really an 
alcoholic psychosis at all, but that the condition is provoked by 
some unknown factors, possibly disturbances of metabolism for 
which the alcohol is only a preparation. But that may be more 
or less true of the whole group. At any rate the symptomatic 
analogy between the different forms is strong evidence that the 
etiological factors are the same or very similar, whatever those 
factors may be. 

To return again to the group as a whole, Kraepelin states 
the situation thus: “ A glance over the forms of alcoholic psy¬ 
chosis just described seems to indicate the possibility of the 
development under the influence of that poison of two different 
groups of symptoms; on the one hand the delirious disturbances 
of retention and grasp, on the other hand the hallucinations and 
delusional formation. The first group of disturbances is present 
among the acute alcoholic manifestations and in simple chronic 
alcoholism ; the latter group is not. This might suggest that in 
the former case we are dealing with the real and essential effect 
of the alcohol; in the latter case with the action of some inter¬ 
mediate factor." But it is difficult to see in this statement what 
provision has been made for the conditions of irritability, ill- 
humour, suspicion, etc., which are such prominent features 
throughout the entire group. Further, in our ultimate analysis 
of the cases, it is not so much the fact that the patient has 
delusions and hallucinations which is significant, as the fact 
that these latter have a definite character. In harmony with 
the patient’s apprehensive state they might be depressing or 
terrifying; dependent upon the clouding of the sensorium, the 
hallucinations may be panoramic, or consist of familiar experi¬ 
ences ; under certain conditions the ideas may be of an expansive 

We find, then, in alcoholic psychosis two groups of symp¬ 
toms, tbe first being conditioned by the apprehensive affect, and 
consisting of depression, restlessness, sleeplessness, irritability, 
anxiety, apprehension, suspicion, depressing or persecutory delu- 



sions, depressing or terrifying hallucinations; the second being 
conditioned by psycho-sensory anaesthesia, and consisting of dis¬ 
tortion of impressions, defective retention, euphoria, carelessness, 
fabrications, occupations, and fantastic hallucinatory experiences. 

In regard to delusions and hallucinations of an expansive 
character, we might expect to find these dependent upon the 
euphoria of cases with memory defect. As a matter of fact they 
do occur: but the more pronounced instances of euphoria usually 
occur with rather grave loss of memory, and these patients are 
obviously not in a condition to develop and maintain a delusional 
system of any complexity. An expansive trend has been 
observed in a number of cases, associated with evidence of pro¬ 
nounced anatomical changes in the brain, such as unequal pupils 
and speech defect, but in which the examination of the spinal 
fluid has shown no lymphocytosis. In these cases the differen¬ 
tial diagnosis from general paresis is a difficult problem. 
Another group presenting expansive ideas may be illustrated by 
the record of a case. 

A. K., woman, aged 54, chronic valvular cardiac disease. 
Father was not entirely right, and paternal cousin was insane. 
Patient is very intemperate; she has had at least six previous 
admissions to this hospital, and has been in the workhouse a 
number of times. In her previous records we find statements 
like the following: Talks incoherently, despondent, noisy, abusive 
and assaulting—the doctors at B. Hospital have taken her heart 
out and mixed up her brain—tells a disconnected story to the 
effect that her husband gave her poison, tells of abuses at B., 
and how the ambulance tells a story about her. She has the 
physical symptoms of general paresis; she has delusions of great 
wealth and importance, thinks she owns a great deal of property, 
has millions of money in the bank, is one of the richest people 
in New York; she hears the voices of her dead relatives and 
sees them; says: “ I have seen God in reality ”; talked in a 
rambling strain, silly, confused, and excitable; noisy and excit¬ 
able ; says : " I have seen the Blessed Virgin and our Lord in the 
workhouse.” At the workhouse she had delusions of persecution, 
of men entering her cell at night, fancied herself imposed upon 
by the other prisoners, whom she accused of conspiring against 
her. The above statements are selected from her various previous 
records. The delusions of persecution are strongly suggestive of 



an alcoholic etiology, but the picture as a whole is not very 
typical of any psychosis. From each of the attacks she so com¬ 
pletely recovered as to be discharged in her own custody. It 
most; however, be borne in mind that alcohol usually destroys 
the body before the mental symptoms have become so prominent 
aa they are in this case. When a patient fifty-four years of age 
has had six previous attacks, the first being twenty-six years ago, 
has a bad cardiac lesion, and is yet alive to tell the tale, we 
must suspect a special vulnerability of that mind, a certain definite 
predisposition. What that predisposition is, is suggested by the 
course, which reminds us of manic-depressive insanity. From 
her record of her present stay in the institution we glean the 
following statements: Sings occasionally, seems alert, elaborates 
with all manner of details and rambles from topic to topic; her 
husband tried to kill her, she has about twelve million dollars 
left by her Uncle Sage, is one of Queen Victoria’s daughters, 
a there she is behind you ” (pointing to the nurse), is a relative 
of King Solomon, he was up at North Brother’s Island. Her 
productions are well illustrated by the following: (Are you 
happy or sad ?) “ I feel happy, if it is a person that I like to see 
them near me, I never was happier than the four years I was a 
patient here. I could go to the laundry and go to bed, and if 
there was an entertainment I was invited, I never cared for 
entertainments, if I could have one of those little Bibles I could 
read, I didn’t care about entertainments because I don’t like 

This production is significant. The alcoholic may be voluble 
on the subject of his delusions, but when a patient is voluble on 
all sorts of indifferent subjects, and pads out his narrative with all 
manner of irrelevant details, we usually find, as in this case, bad 
heredity, a history of previous attacks with complete recoveries, 
other manic traits, often delusions of grandeur ; and the cases go 
on to recovery without residuals, as the case under consideration 
has done. A number of alcoholics with expansive ideas are of 
this type: the alcoholic manic will spin long yarns about his 
immense wealth the same as any other manic. 

In differential diagnosis we must consider the fact that only 
a very small percentage of the population of our cities are total 
abstainers. In many families alcoholic beverages are upon the 
bill of fare more or less regularly. With the onset of a psy- 



chosis, many formerly temperate persons begin to consume 
excessive amounts of alcohol, tea, coffee, or tobacco. With the 
development of a psychosis, many patients become also very 
intolerant of alcohol, and thus seem more intemperate than they 
really are. The relation of the patient’s habits to the onset of 
the psychosis is important in determining to what extent in¬ 
temperance is an etiological factor, and to what extent it is a 

The differential diagnosis between certain forms of alcoholic 
psychosis and Dementia Prsecox merits our special attention. 
If there is to be such a group as alcoholic insanity, we might 
hope to find something common to that group. These common 
features have been already pointed out. If we are to recognise 
any such group as Dementia Prsecox, there should be also some¬ 
thing common to that group. Kraepelin mentions as an im¬ 
portant diagnostic point the loss of interest. In addition, there 
is a striking feature, which, if not common to the entire group, 
is at least sufficiently general to be of much assistance to us, 
viz. the absence of obvious cause and effect relations. Not 
but that cause and effect relations are operative, the same as 
everywhere else in creation, but they lie too deep for our present 
methods of psychologic analysis. For instance, the alcoholic is 
depressed for definite reasons; whether it is the persecutions of 
his neighbours, the infidelity of his wife, or the snakes under the 
bed, there are in any case definite and adequate reasons. The 
complaints of the precocious dement, on the other hand, are 
indefinite and incoherent, are a mere jumble of odd notions, 
cannot be written out in orderly sequence, are difficult of 
expression, unintelligible, often cannot be represented in thought 
by the normal individual at all, and are totally inadequate to 
explain the state of mind. In conduct the alcoholic may be 
resistive from suspicion, negativistic from sulkiness, assaultive 
upon provocation, real or supposed. The resistiveness and 
negativism of the precocious dement are in response to a blind 
and unreasoning impulse, for which the patient gives no adequate 
reasons. We must, however, differentiate obsessions, which are 
quite a different phenomenon, and distinguished by the fact that 
the patient has insight. This feature, the absence of adequate 
cause and effect relations, may be expressed as inconsistency or 
incongruity. If we then bear in mind as the common features 



of alcoholic psychosis, apprehensiveness and disturbance of 
grasp, and the common features of Dementia Prsecox as incon¬ 
gruity and loss of interest, we shall be in a position to size up 
our cases intelligently. 

The record of a case is here presented by way of illustration. 

B. M., aged 27, heredity negative. Had chorea as a child, 
later lived out; trifles disturbed her; at times would be so 
absorbed as not to listen to what was said to her; had few 
friends and no love affairs ; was stated to be alcoholic. Was in 
this hospital six years ago and presented an atypical clinical 
picture: is said to have recovered completely. After that time 
she did not drink at all until lately. Six months ago patient 
gave up her place, went to church twice a day in order to save 
her soul. Two months ago was worried over her brother’s 
drinking habits, and thought he was going to die. For the last 
month she has taken much alcohol. Informant sometimes gives 
her brandy to get her to sleep. Before admission she saw the 
Virgin; thought the devil was coming, and heard voices calling 
to her. In the hospital she said: “ Oh, Jesus, Mary, and Joseph 
—Jesus, Mary, and Joseph—I don’t want to be killed—I don’t 
want to die—-Jesus, Mary, and Joseph—Miss K, don’t leave me.” 
(Tell me what you are thinking about ?) “ I don’t know how I 

feel—I feel pretty well—I am thinking of God and of Hell— 
I am thinking of—oh, I guess I will be all right.” (What are 
your ideas ?) “ I am thinking I am going to die—I would like 

to make amends for my sins—I did not do very much sin—and 
I guess God will forgive me—I might have done a good 
deal. ... I feel things, that is all—I feel things ahead of me 
—I cannot say what they are—I want to die and go to Heaven 
—if it is God’s will I would like to live and be good—very 

The following is an extract from the description of her con¬ 
duct : It is almost impossible to get her to make an attempt to 
write. She gets up, looks anxiously about her, says: “ Oh, 
Mary and Jesus,” finally takes the pen in her hand and says : 
44 Must I write—Yes ! I will write—I can’t write.” She takes 
up the pen and lays it down two or three times, approaches the 
paper as if to write, then says : “ I will not.” After about ten 
minutes of parleying she writes her name. She is asked to 
write one of the test phrases, and the same performance is begun 



again. Finally the attempt to get her to write is abandoned; 
she then becomes rather resistive, refuses to give up the pen, 
and says: “ I will write.” The paper is put away, and she 
reaches for it, puts it back in place, writes two words, misspelling 
them, then she begins to parley again. Similarly in the ward 
later, if asked to wait on table she offers to wash the dishes; if 
asked to make the beds she offers to polish the floor; ultimately 
does nothing. She has also committed assaults, for which no 
motive could ever be elicited. Her orientation is approximate 
as to many of the bare facts, but she shows her loss of the 
higher mental functions by her failure to grasp the significance 
of her situation. 

Now it is impossible to analyse the wail of this patient and 
to state in definite terms what it is that is weighing on her 
mind. Her complaints are contradictory, vague, confused, and 
groundless. In her conduct she shows the conflict of ideas and 
impulses which has been much emphasised by the writers on 
Dementia Prsecox. It is but a special manifestation of that 
incongruity discussed above. The patient is willing enough to 
co-operate, and yet for no obvious reason fails to do so. No 
explanation was given for her tendency to assault. Her inability 
to construct the situation seems to be dependent, not on defective 
grasp, but on failure of interest and attention. All this, with the 
fact that she seems to have been temperate until the beginning 
of the psychosis, and with several other suggestive features, 
establishes the diagnosis of Dementia Prsecox. The alcoholic 
indulgence may have had something to do with the apprehensive 
state of the patient upon admission, although these states are 
common enough in Dementia Prsecox. This view of the case is 
borne out by the subsequent course. Her apprehensiveness soon 
quietened down, but aside from that her mental state is the same 
as upon admission. 

In sizing up these cases we have to make allowance for the 
extension of the process to contiguous fields. To take an example : 
as a result of the impairment of retention, there occurs a loss of 
memory, and then this amnesia may go back five or ten years 
before the beginning of the psychosis. Similarly a case of 
Dementia Prsecox may show a primary loss of interest, and with 
that a profound loss of memory due to the failure to take notice. 
In many cases the reasons for the extension of the process are 



much less obvious. Localised brain lesions are accompanied by 
psychologic phenomena impossible to account for. This empha¬ 
sises the importance of studying the mechanism wherever that 
can be traced. In this connection special importance must be 
assigned to the initial symptoms of the disorder, and to the 
dominant symptoms at the time the patient is under observation. 

Here the question might be suggested: Is not a case of 
Manic-Depressive Insanity or Dementia Prsecox, provoked by 
alcohol, usually also coloured by alcoholic symptoms ? That 
does not infrequently occur, though probably not as often as is 
usually supposed. The case usually shows a fairly clean cut 
picture of either one psychosis or the other. The explanation 
seems to be that if the mind has a predisposition towards some 
certain psychosis, it breaks down in that particular direction 
before the patient has consumed enough alcohol to give him 
very many of the characteristic alcoholic features. This reminds 
us of the observation that very few of the pathological changes 
due to alcohol are found post-mortem in hospitals for the insane 
as compared with the findings in general hospitals, due to the 
fact that these patients break down mentally before they have 
consumed enough alcohol to make its effects apparent in the 
parenchymatous organs. 

The differential diagnosis of the Paranoic conditions requires 
but a brief mention. The term Paranoic condition is but a small 
part of a diagnosis, though it may be all that certain cases will 
justify. It simply states the fact that the patient has accumu¬ 
lated in some way a certain number of fairly coherent morbid 
ideas, but it is non-committal as to the nature of the process. 
Some Paranoic trends are developed in the course of chronic 
hypomanic states; sometimes we find that dream-like experiences 
have played an important part, and the process seems analogous 
to certain forms of Dementia Prsecox. The differential diagnosis 
of the alcoholic Paranoic states, so far as it is possible, is to be 
made largely from the history of the development. 

The mechanism of the development in a senile psychosis is 
practically the same as that of an alcoholic psychosis. The 
cases show the same defective grasp, the same affability, the 
same disorientation, the same fabrications, an analogous occupa¬ 
tion delirium, and analogous persecutory ideas. The differential 
diagnosis of a doubtful case resolves itself into a rather unprofit- 



able discussion of the question as to what extent intemperance 
has hastened the usual processes of decadence. In fact, alcoholic 
insanity seems to be a member of a larger group including in 
addition, senile psychoses, polyneuritic psychosis due to other 
causes, and certain traumatic cases. It is possible that these 
represent a special type of reaction, but more likely that the 
correlation between certain of the forms might be made upon 
anatomical grounds. 

The relation of alcoholic insanity to Manic-Depressive Insanity 
and to Dementia Praecox is quite different. It may be that the 
symptomatic differentiation between certain cases of alcoholic 
insanity and certain cases of the Paranoid form of Dementia 
Praecox may be rather indefinite. Those cases offer a promising 
field for comparative study. But with that possible exception, it 
may be stated that the conditions are quite different. It is 
generally conceded that intemperance may provoke an attack of 
either Manic-Depressive Insanity or Dementia Praecox in indi¬ 
viduals with a special predisposition, acting in the same way as 
any other debilitating factor. But the term alcoholic insanity is 
used to designate the manifestations of that poison in individuals 
of approximately normal mental make-up. The clinical picture 
is very definite, the condition is well entitled to recognition as a 
distinct disease-entity, the mechanism of the process is some¬ 
thing fundamentally different from that of either Manic-Depressive 
Insanity or Dementia Praecox, and the conditions are not to be 

To recapitulate briefly: The symptoms of alcoholic insanity 
group themselves round two fundamental elements, apprehensive¬ 
ness and defective grasp. In cases which do not yield to an 
analysis on this basis, some complicating factor must be sought. 
The symptomatology of the first stage of intoxication is very 
complex, but the primary disturbance seems to be defective 
grasp with consequent euphoria ; the second stage is characterised 
by apprehensive symptoms. The anomalous forms of intoxication 
show the same features, and in addition the manifestations of a 
morbid predisposition. Acute hallucinatory insanity is a very 
pure form of psychosis dependent upon the apprehensive state of 
the patient. The polyneuritic form shows symptoms dependent 
on, or related to, both the fundamental symptoms referred to 
above, but is characterised as such by disturbance of grasp of a 



special type. The chronic alcoholic shows symptoms of both 
series. The Paranoic states are gradually developed in chronic 
alcoholics, usually with the assistance of hallucinations, or are 
residuals of otherwise recovered acute forms. Alcoholic stupor 
is dependent probably upon anatomical changes in the brain. 
Periodic alcoholism is often the result of a constitutional dis¬ 
position. Alcoholic deterioration is to be recognised by the 
character of its mechanism. Delirium tremens is closely allied 
to the polyneuritic psychosis, but represents a much more pro¬ 
found disturbance. An expansive trend may depend upon the 
euphoria associated with psycho-sensory anaesthesia; it occurs 
also in alcoholic pseudo-paralysis, and in alcoholic manics. 
Alcoholic insanity is analogous in its mechanism to senile 
psychoses, to the polyneuritic psychosis due to other causes, and 
to certain traumatic psychoses, but is fundamentally different 
from Manic-Depressive Insanity and Dementia Praecox. 



Commissioner in Lunacy for Scotland. 

A good deal of objection has been raised against the use of this 
term by Kraepelin, chiefly on the ground that Dementia has 
acquired a definite meaning, connoting, among other things, an 
incurable condition. It may be at once admitted that so far as 
concerns English terminology at any rate, the name is un¬ 
fortunate, though by no means so confusiug as is alleged. The 
use of the term in German gives rise to no embarrassment, for it 
does not conflict with the word “ Blodsinn,” the usual term for 
Dementia as we understand that word. It would perhaps be 
better for psychiatry in our own country if less attention were 
directed to the name, and a little more criticism devoted to the 
substance of the entity which Kraepelin has presented to us 
under the name of " Dementia Praecox.’’ Is there such a clinical 
entity, and are its three sub-forms so intimately related as to 
justify their being classed together under that or any other 
name ? These are, after all, the important questions to consider. 
If they can be answered in the affirmative, then we possess the 
most important advance in clinical psychiatry which has been 



made in recent times. If they must ultimately be answered in 
the negative, the name is of small consequence, for it must pass 
away along with the erroneous idea which it denotes. Before 
passing from a consideration of the name, let me remark that it 
is not so wholly inapplicable as many persons would have us 
suppose. The condition as described by Kraepelin possesses, at 
any rate in its terminal stages, many points of resemblance to 
ordinary dementia; and 90 per cent, of the subjects remain 
permanently crippled in mind and go to form a very considerable 
proportion of the demented population of our asylums. 

I have been frequently struck with the fact that among the 
many criticisms of Kraepelin’s presentation there has been but a 
scanty attempt made to describe his main propositions in his 
own words. To do so at length would involve, practically, a 
translation of a long portion of his text-book, but I have resolved, 
in the interests of clearness and fairness, to present here an 
epitome of the basis upon which he founds his argument for the 
existence of the clinical entity which, whatever may ultimately 
be thought of it, is at present profoundly influencing current 

At the outset of his description, Kraepelin admits that the 
variety of clinical forms included under the generic term 
Dementia Praecox is very great, and that to a superficial observer 
the connection between them may not be readily perceptible. 
Yet there are certain basic symptoms underlying the more 
transitory appearances of the disease processes which all cases 
suffering from the affection possess in common. 

(1) There is first the peculiar form of stupid listlessness 
from which one might conclude that the patients were oblivious 
to circumstances and events in their environment. On the con¬ 
trary, however, the patients are able to appreciate and to, on 
occasion, describe everything that happens in their surroundings. 
They are able to tell where they are, to recognise individuals, 
and to count with accuracy. Only in profound stupor, and in 
the graver melancholic conditions, is orientation at all affected ; 
yet in spite even of these serious mental disturbances the 
patients often remain clear in this respect. It is only when the 
thoughts of the patients are seriously affected by delusions that 
orientation and the perception of the surroundings are gravely 
interfered with. 



(2) The sensory sphere is liable to grave implication, which 
often commences with dream perceptions. Hallucinations of the 
senses occasionally accompany the whole course of the disease; 
oftener they fade entirely, only to return with renewed force in 
the later stages of the disease. The hallucinations are at first 
of an unpleasant nature and very vivid. Later on they are 
regarded by the patients with more equanimity, and a few are 
even diverted by them. 

(3) The consciousness of the patients, except in the excited 
and stuporose conditions, remains perfectly clear. More severe 
disturbances, however, not infrequently result in an affection of 
die faculty of attention, which is most apparent when an effort 
is made to sustain a conversation upon one topic for any time. 
On the other hand, it is not infrequent to see such patients 
observe stealthily what goes on around them, look curiously in 
at open doors, follow people at a distance, and manifest generally 
a sort of morbid curiosity in their surroundings. 

(4) Memory is, proportionately, but little disturbed. The 
patients can, if they wish, give correct accounts of all past 
events in their experience, and even up to the time of the 
occurrence of the deepest dementia, retain all they have learned 
at school with astonishing tenacity. After severe stupor it 
generally happens that the memory is confused and weak, but 
that readily passes oft' in a few days or weeks. 

(5) Sooner or later the thought processes of the patients 
always undergo deterioration. In milder cases this is shown 
merely in an increased abstraction of thought or in an unadjusted 
passing from one set of ideas to another. In more severe cases 
the affection manifests itself by incoherence of speech, with verbi¬ 
geration or new word formation. But it has to be remembered 
that, in spite of these outward symptoms of thought disorder, the 
patients still preserve a fairly firm grasp of their surroundings, 
and that they can adjust themselves in a surprising manner to 
their environment. The presence of the peculiar phenomenon 
known as “ Stereotypism ” is almost always present as a symptom 
of the disordered thought processes. It results from the domin¬ 
ance of special ideas which for weeks and months at a time 
forcibly possess the mind, and frequently show themselves as 
repetition of senseless words, rhymes, or a strained play upon 
the superficial connection between words. 



(6) The judgment of the patients is always without excep¬ 
tion affected. They are incapable of acquiring new experiences, 
and so soon as they find themselves in novel and strange cir¬ 
cumstances they become helpless. They are unable fully to 
comprehend that the change is in themselves and not in their 
surroundings, consequently they form erroneous and false con¬ 
ceptions of their position. 

(7) Upon this basis, delusions of a fleeting or lasting nature 
are apt to arise. In the early stages of the disease the contents 
of the delusions are sad or hypochondriacal. Later on, grandiose 
ideas begin to appear, which may gradually become dominant. 
As a general rule, and owing to the rapidly developing mental 
weakness, all forms of delusion exhibit a nonsensical, quixotic 
stamp. They are, moreover, not constant, but change their 
character from time to time in accordance with the mental con¬ 
dition of the subject. In the Paranoid form of the disease the 
delusions present a more lasting character, but even there they 
ultimately become incoherent and dissociated. The tendency 
for all these delusions is ultimately to disappear in forgetfulness. 

(8) The mental disposition undergoes marked change. At 
first the patients are depressed, which condition is varied by 
outbursts of excitement or of unrestrained joviality. Next 
follows a state of good-natured dementia, which is accompanied 
by a peculiar listlessness, a loss of affection for relatives and 
friends, and a disinclination for employment or recreation. They 
seem to experience neither pleasure nor pain, to exhibit neither 
desire nor apprehension, but live for the day only in a dull and 
stupid manner. They also manifest indifference towards bodily 
discomfort and slight pain; the only interest or pleasure that 
remains is that for food. Towards the later stages of the disease 
a condition of complete listlessness supervenes, varied occasion¬ 
ally by outbursts of irritability. 

(9) The behaviour of the patients adds importantly to the 
clinical picture. They lose all power of initiative and neglect their 
work and their obligations. Along with this loss of initiative, 
there is displayed passing or lasting impulses towards suicide. 
The impulse to self-destruction does not imply any increased 
initiative on the part of the patient, but is only a result of a 
motor excitement which impels to destroy. These impulses are 
aimless, and are due to the sudden relaxation of the previous 



inhibitory tension under the influence of excitement. All the 
impulses are equally aimless, such as the breaking of windows 
and dishes, as well as attempts at self-mutilation. All the 
common actions of the subjects, such as walking, writing, eating, 
hand-shaking, are apt to be traversed and interrupted by impulses. 
In this way are exhibited those mannerisms and peculiarities 
which are so characteristic of the patients. 

(10) To this affection of the will power, coupled with the 
prevalence of automatic impulses, is attributable that peculiar 
negativity which manifests itself as an obstinate opposition to 
every change of position, to taking food, to putting on or off 
clothing, etc.; to the same cause is due the retention of urine, 
faces, and saliva, the creeping under beds, the refusal to answer 
questions, the “ touchings,” and the general inaccessibility to all 
attempts at approach on the part of others. This negativity 
which can seldom be influenced from without, may yet through 
some internal impulse be suddenly counteracted and the 
patient may all at once engage in some useful or senseless 
piece of work, only, however, to fall back again into his former 

(11) The working capacity of the patients is without 
exception lowered and may be seriously affected. Their work has 
to be carefully supervised, for they stop at the slightest difficulty, 
and should they meet with anything novel or unusual, they are 
incapable of adapting themselves to the altered condition. In 
the performance of artistic work, to which they may have been 
previously trained, they manifest along with, it may be, great 
technical ability, a failure in the sense of beauty and proportion, 
and a decided inclination towards peculiarities. In musical 
patients the decay of the finer artistic feelings is early manifested, 
and exhibitions of a distorted and capricious nature are the 
general rule. 

In addition to the above list of mental symptoms, which are 
common to all forms of Dementia Prsecox, Kraepelin mentions a 
series of bodily symptoms which be admits have not been estab¬ 
lished and correlated, but which are sufficiently important to be 
hriefly detailed. 

(1) In about 18 per cent, of all cases he has observed the 
occurrence of epileptiform or tetanic spasms, or even of apoplecti¬ 
form attacks followed by more or less transient paralysis. All 



such attacks are twice as numerous in the female as in the 
male sex. 

(2) Choreiform movements of a special and lasting character 
have been repeatedly observed. 

(3) The tendon reflexes are regularly exaggerated, often 
markedly so; there is also often an increase in the mechanical 
excitability of the muscles and nerves. 

(4) The pupils are often widely dilated, especially in the 
excited stages of the disease ; here and there one observes a 
difference in the relative sizes of the pupils. 

(5) The heart’s action is subject to great irregularity, some¬ 
times slow, often accelerated, at other times weak and irregular. 
Vasomotor changes of all kinds are common. 

(6) The sweat and salivary secretions are liable to be greatly 
increased in certain patients and at certain stages of the disease. 

(7) Diffuse enlargement of the thyroid gland has frequently 
been noted prior to the onset of the mental symptoms, and it has 
been noted to return quickly at the circumference of the gland 
during the development of the malady. In a few cases distinct 
exophthalmos was present. Finally, among the histories of the 
relatives of the patients it is not uncommon to find rayxoedematous 

(8) The sleep of the patients is invariably disturbed. 

(9) The body weight, irrespective of the quantity or quality 
of the food taken, is liable to great variation, depending upon the 
recurrence and subsidence of the acute attacks. When per¬ 
manent dementia ensues and the acute attacks cease, it is usual 
to find the patients take on flesh and present a well-nourished 

The three divisions of Dementia Prsecox, according to 
Kraepelin, are : Hebephrenia, Katatonia, and Dementia Paranoides. 
He defines each shortly as follows: “ By Hebephrenia is meant 
all those forms of Dementia Prsecox in which a uniform, more or 
less profound condition of mental weakness is developed under 
the accompanying influence of subacute—more seldom of acute 
—mental disturbances.” 

“ Katatonia is essentially a peculiar disease process progress¬ 
ing through stupor or excitement to a condition of dementia, 
with intercurrent symptoms of Negativism, Stereotypism, and 
Auto-Suggestibility in the spheres of action and work.” 



“Dementia Paranoides includes a group of cases in which 
delusions and hallucinations are produced in an otherwise dear 
mind throughout many years of a steadily advancing mental 

That these divisions are largely artificial is candidly admitted 
by the author (vide “Lehrbuch,” pL il p. 148, 6th ed.). “There 
can,” he says, “ be no rigid line drawn between the divisions, 
because the cases run into each other and overlap continually. 
There are a whole series of recurring forms, but between them lie 
such a variety of transition cases that, in spite of all effort, it is 
impossible to classify each case, without exception, in a given 

In forming an estimate of Kraepelin’s conception of Dementia 
Prsecox, as I have attempted to present it above, largely in his 
own words, it is necessary to approach the subject from the 
point of view of the author and of those who agree with him, 
Up to within the last two decades of the nineteenth century the 
progress of psychiatry was somewhat slow and shadowy, especially 
in the field of pathological research. The great pathological ad¬ 
vances of the last twenty-five years have not as yet very markedly 
affected the clinical side of the study of mental diseases. Con¬ 
sequently classification is chaotic. There may not be much harm 
in that so far as individual physicians are concerned, for long 
practice endows the physician with an empirical knowledge, 
which, however, perishes with himself. The great want has been a 
nomenclature or language by means of which each earnest, educated 
physician can communicate his empirical impressions to others. 
This Kraepelin has done effectively in this instance. It may be 
that the language, or perhaps I ought to say the words, are 
uncouth, but the idea underlying them is a living reality. Out 
of the unutterable confusion of psychiatric nomenclature Kraepelin 
selects a group of cases—not a large group, only about 15 per 
cent, of the total annual admissions to his Clinique—he predicates 
certain things regarding their symptoms, diagnosis, and prognosis, 
and asks his brethren throughout the world to criticise his 
position. These patients were previously unattached, so to speak; 
each man classified them variously according to his own peculiar 
views, with the result that our knowledge was becoming hazy in 
respect to the prognosis of various types of acute insanity. 

The great importance, then, of Kraepelin’s presentation of 



Dementia Precox lies in the essential advance he has attained 
in the prognosis of a hitherto unclassified group of cases. In 
this group a progressive mental weakness is the constant and 
leading feature. But progressive mental weakness alone does 
not constitute Dementia Precox. There are other symptoms 
which enable the physician from an early stage of the disease to 
form an unfavourable opinion as to its course. These symptoms, 
which have already been detailed, are Negativism, Peculiar 
Mannerisms, Stereotypism, Impulses (Willensstorung), and especi¬ 
ally Disorders of Judgment (Urtheilsfahigkeit). Strongly con¬ 
firmatory of Kraepelin’s position is the fact that these symptoms 
are common to a large number of so-called terminal dements. 

It is an objection of considerable force that a certain pro¬ 
portion of the group make satisfactory recoveries—8 per cent, 
according to Kraepelin himself. The only possible answer is that 
our knowledge is not sufficiently advanced to enable us to dis¬ 
tinguish allied types which are not really cases of progressive 
dementia from those which are. 

Some objection has been raised on the ground that the con¬ 
ception is neither pathological nor etiological. This is a futile 
objection when our knowledge allows us to supply neither the 
one nor the other. The classification is at any rate thoroughly 
clinical, and its merit depends upon the valuable aid it affords in 
prognosis, which is, after all, the most important detail in 
psychiatric medicine at the present day. Should it be estab¬ 
lished that these affections, or some of them, depend upon a 
toxic basis, as Dr Lewis Bruce hopes to be able to substantiate, 
we shall not even then have fully solved the mystery. It must 
be remembered that in many instances Dementia Precox is a 
slowly progressive disease, extending over many years; that it 
often occurs in individuals who have for some reason failed to 
develop properly either mentally or physically; and that its com¬ 
mencement may be insidious and unobserved. We must look, 
therefore, for some other reason than a toxic causation alone. 
Keeping in mind Kraepelin’s observations upon the changes in 
the thyroid gland in some of his patients, as well as other facts 
in development, it is not unlikely that physiology has yet much 
to teach us regarding the influence of various bodily glands upon 
nervous mechanism. 

In concluding these remarks, I may perhaps be pardoned for 



pointing out that the opponents of Kraepelin’s conception of 
Dementia Pnecox write and speak as if it were put forward as 
an ultimate solution of the problem of psychiatric classification 
which threatens to darken counsel for all time coming. This 
illusion of finality may have its uses in many departments of 
life, and even in some of the more exact sciences; but it is 
surely misplaced when applied to psychiatry, which is now in 
a state of fiux and change in all its branches. The truth is that 
Kraepelin himself would be the last man to assert that his con¬ 
ception was more than tentative—except, of course, as regards 
diagnosis and prognosis. He has handed on the torch and even 
trimmed it. His very errors will form a necessary step in the 
progress of our knowledge. In the meantime many of the lead¬ 
ing alienists in both continents have accepted his presentation 
as a simple, workable advance, the outcome of genius and of 
incalculable patient observation. 

Notb.—T he Editors have requested that I should, for the benefit of the 
non-psychiatric reader, explain some of the unusual technical terms which 
occur in this paper. I gladly do so with apologies for their use. 

Hebephrenia (Ipy, puberty ; mind), lit., the mind of youth. 

Katatonia (*arareiiw, I stretch tightly) is applied to this disease because 
of the cataleptic rigidity which frequently accompanies its stuporose phases. 

Dementia paranoides. Paranoia (rapa, beyond; roiw t I know) is a term 
now usually applied to delusional insanities. 

Stereotypism is a term applied to designate the expression of recurrent 
phrases which are the outward signs of certain fixed ideas which dominate, 
for longer or shorter periods, the minds of the patients. 

Verbigeration means the repetition of sounds or words, often meaningless 
words, invented by the patient himself. 

Negativism implies a state of chronic resistance on the part of the patient 
to conform to the necessary conventions of life. 

Auto-suggestion is used to describe the presence in the mind of obsessions 
or independently arising suggestions which precede and lead up to the 
innumerable impulses in action which are a leading feature in the sympto¬ 
matology of the disease. 






(85) Arb. a. d. neurolog. Institut a. d. Wien. Universitat, Bd. 13, S. 25. 


(86) KANDL, Ibid., S. 141. 

Both these papers are devoted to description of the minute 
morphology of these cerebral fissures and gyri in the lower and 
higher apes and in man. As such, suitable abstracts cannot be 
easily made of their contents, and those interested in the subjects 
must be referred to the original articles. 

It may be noted, however, that in the first paper annectant 
gyri (G. cuneo-linguales) are described in the calcarine fissures of 
some of the higher apes, though Cunningham has regarded them 
as peculiar to the human brain. 

In the same paper the question is discussed in how far the 
F. calcarinse of the simian and human brains are homologues. 
According to Cunningham the F. cal carina of the monkey corre¬ 
sponds to the auterior limb of the calcarine fissure of man, while 
Elliot Smith believes it is represented only in the posterior limb. 
Zuckerkandl rejects both these views and regards the human and 
simian calcarine fissures, each as a whole, as true homologues. 

Gordon Holmes. 


(87) (Vergleichend-anatomische Untersuchungen liber den Ban dee 
Zentralkanales bei den S&ugetieren.) P. Biach, Arb. a. cl. 
neurolog. Institut a. d. Wien. Universitat, Bd. 13, S. 399. 

The central canal of the spinal cord has been investigated by the 
author in representatives of almost all the mammalian classes. 
He finds that in the lower mammals, in contrast to man, it is 
almost always elliptical in cross-section, its greatest length lying 
in the dorso-ventral axis of the cord. It is always exactly in the 
centre of the lateral diameter of the cord ; in the cervical segments 
it generally lies in the centre of the commissure, but in the dorsal 
and sacral segments in the ventral half of the commissure, owing 



to the increased breadth of the dorsal half of the latter. In almost 
all classes (the natantia are an exception) it has a distinct lumen 
which contains a granular, felt-like, or homogeneous material, in 
which cells of glial or ependymal origin or even leucocytes are 
often embedded. In many specimens a homogeneous structure, 
round on cross-section, was found within the canal This is the 
structure which has been described as Reissner’s fibre, but Biach 
agrees with Studnicka that it is not a nervous structure, but pro¬ 
bably only a coagulated deposit within the canal. The ependyma 
that lines the canal generally consists of a single layer of cubical 
cells, from the dorsal and ventral surfaces of which bundles of 
glial fibrils radiate into the substance of the cord. 

The substantia gelatinosa centralis has no definite boundaries. 
It consists of a dense network of neuroglial fibrils, and nerve cells 
and fibres are frequently found within it. Its size is very variable 
in the different orders. In some of the lower mammals it extends 
along the median border of the dorsal horns to become continuous 
with the substantia gelatinosa Rolandi; in other orders in which 
there is no continuity between them their identity is indicated by 
the presence of similar cells in each. Besides the few myelinated 
fibres which extend into it from all sides, the substantia gelatinosa 
centralis almost invariably contains in the lumbo-sacral segments 
snail bundles of longitudinally running fibres which can be 
followed into the tip of the conus. Gordon Holmes. 

( 88 ) WITH THE VAGUS. (Ueber die intrabulbaren Verbindungen 
das Trigeminus sum Vagus.) M. Grossmann, Arb. a. d. 
neurolog. Institut an Wien , Bd. 13, 1906, S. 194. 

From his experiments on the effect produced on the heart by 
stimulation of the central end of the V., and on the effect of the 
nasal reflex on the circulation and respiration, the author came 
to the conclusion that there is a direct functional connection 
between the V. nerve on the one hand, and the vagus and phrenic 
nerves on the other. Stimulation of the central end of the V. 
raises the blood pressure and influences the rhythm of the heart 
and the movements of the diaphragm. 

A direct anatomical connection between the trigeminus and 
the vago-glosso-pharyngeal nuclei has been already described. 
Wallenberg found, in a case in which the sensory root of the fifth 
was degenerated, a special bundle lying in the dorso-medial angle 
of its spinal root which could be followed into the tractus solitarius; 
and Bruce and Hagelstamm found changes in the latter after 



degeneration of the sensory root of the trigeminus. Cassierer and 
Schiff found this bundle intact despite destruction of the IX. and 
X. nuclei, and were able to trace it upwards to the sensory nucleus 
of the V. Lewandowsky has denied the existence of any such 
connection between these two nuclei, as he was unable to discover 
it in his experiments on monkeys. 

The author’s experiment consisted in the removal of the 
Gasserian ganglion in a monkey and the subsequent examination 
of the brain-stem by Marchi’s method. He obtained complete 
degeneration of the sensory V. root; some of its fibres entered the 
cerebral root, others terminated in the motor trigeminus nucleus, 
but the majority ended in the sensory nucleus and in the spinal 
root. No direct root fibres passed to the cerebellum. 

At the caudal end of the sensory nucleus a small collection of 
cells, to which the name nucleus ovalis is given, was found lying 
at the dorso-medial angle of the spinal root and its substantia 
gelatinosa Rolandi. It seems to be a continuation of the sensory 
nucleus, and its cells resemble those of it rather than those of the 
substantia Rolandi. It is surrounded by degenerated fibres, some 
of which end in it and others pass to it from the spinal root. 
Further caudal wards it moves dorsalwards and lies embedded in 
the ventro-medial angle of the spinal root of the vestibular nerve, 
and finally it joins the substantia gelatinosa of the fasciculus soli- 
tarius. It is accompanied for its whole length by degenerated 
fibres of the trigeminus. 

These fibres and the nucleus ovalis then represent a direct 
anatomical connection between the trigeminus and the vago- 
glosso-pharyngeal nerves. 11 has been assumed (Roller, Wallenberg, 
Edinger) that the fasciculus solitarius and its cerebral ward projec¬ 
tion belong to the function of taste, but the investigation of 
Cassierer and SchifFs case disproves this view, and Grossmann 
adds that as fibres from all three divisions of the trigeminus enter 
it the nucleus ovalis cannot be only a taste centre. 

Gordon Holmes. 

(89) IN MAN. (Beitr&ge zur Kenntnis der sensiblen Wnrzeln der 
Medulla oblongata beim Menschen.) E Hulles, Arb. a. d. 
neurolog. Institut a. d. Wien. Universitai, Bd. 13, S. 392. 

The author has attempted to determine how far neuroglia extends 
into the roots of the sensory cranial nerves. When the vagus root 
is cut longitudinally as it enters the medulla it is seen that there 
is an interruption of its myeline sheaths a short distance before its 
entry; over a zone about 1 mm. broad its fibres are not stained by 



Weigert’s method. This pale band is convex peripheralwards, and 
by suitable staining it is seen that it is the region where the root 
fibres lose their sheaths of Schwann, and the peripheral limit of 
the extension of the neuroglia of the bulb along the root. In some 
of the nerves (V. and X.), however, irregular projections of neuroglia 
extend further along the nerve. The dense band of glia which 
occupies the area that stains palely by Weigert’s method is con¬ 
tinuous with the marginal zone of neuroglia of the central nervous 
system which extends over the most proximal portion of the root 
as a sheath. The pia mater surrounds the whole and joins the 
connective tissue sheath of the nerve. 

This condition is compared with what Levi has found in the 
posterior spinal roots. The chief difference is that in the cranial 
nerves the baud of neuroglia lies further peripheral and is broader 
than in the spinal roots, and that the latter are not surrounded by 
a sheath of pia mater. 

Hulles also examined the intramedullary portion of the 
sensory roots by Bielschowsky’s method in the medulla of new¬ 
born babes. He failed to find bifurcation of any of the fibres of 
the vagus, but saw a few fibres of the trigeminus branch after they 
had entered the pons. Gordon Holmes. 

(90) FIBEE WITH ITS CELL BOD7. Oliver S. Strong, Journ. 
of Comp. Near, and Psych., Vol. xvi., No. 6, Nov. 1906, p. 397. 

This paper gives some demonstration of the subject title as 
studied in the lumbar cord of an infant, by various modifications 
of the Weigert-Pal method. 

The “axone cone” emerging from the cell body may either 
taper regularly, or first gradually and then more abruptly, to the 
narrow neck of the axis-cylinder process. This attenuation of the 
axone at a point near the cell body has long been known, and may 
be partly an artefact, but is probably not entirely so, as it has been 
demonstrated by so many methods. Beyond it the axone expands 
and at the same place becomes medullated; the expansion and 
myelination seem to be correlated as regards whether they occur 
abruptly or gradually. 

Only one collateral branch was observed from the naked part 
of the axone, but, as the author remarks, this cannot be regarded 
as negative evidence of much weight, for the methods employed 
were incapable of demonstrating very fine processes. For this 
reason the axones of the smaller cells were not available for study. 

J. H. Harvey Pirie. 




John Cameron, Brain, 1906, p. 332. 

The main aim of this paper is to emphasise the importance of 
recognising that the nuclei of embryonic nerve-cells (neuroblasts) 
are centres of great metabolic activity. One of the earliest indica¬ 
tions of the latter is shown in lower vertebrates (e.g. fishes and 
amphibians) by an ingestion of yolk-particles at one definite pole 
of the nuclear wall. For this region the title of assimilative pole 
has been adopted. The ingested yolk is elaborated within the 
nucleus, and stored up as chromatic material, which first shows 
near this pole. 

Still more striking evidence of the existence of this nuclear 
metabolic activity is shown in these lower vertebrates by the fact 
that part, at least, of the earliest rudiment of the axis-cylinder 
process arises in the form of successive extrusions of nuclear 
achromatic substance from the assimilative pole of the neuroblast- 
nucleus. This pole thus becomes the aeon-pole. The assimilative 
or axon-pole of the neuroblast-nucleus has always a definite direc¬ 
tion. Thus it looks towards the ventricular cavity in the cerebral 
hemispheres, and forwards as well as outwards in the anterior 
cornua of the spinal cord. It is found, further, that not only the 
axon-rudiment, but also a considerable proportion of the cytoplasm 
of the future nerve-cell is produced from the neuroblast-nucleus, 
owing to the continued exercise of this achromatin function. 

The material which is extruded is achromatic only in the 
nascent condition. It very soon, however, undergoes a characteristic 
process of rechromatisation, which affects the extruded perinuclear 
substance in a definite manner, and gives rise to the neuro-fibrillary 
network, and probably also to the Nissl bodies. 

It is a significant fact that the neuroblast - nuclei exhibit 
structural changes as evidence of their metabolic activity. The 
most striking is a disappearance of the accumulated chromatic 
material from the axon-pole, which occurs during the period that 
the axon-rudiment is being given off. The chromatic element is 
thus retransformed into nascent achromatic element, in which 
condition it is discharged from the nucleus. 

The results of this research go to show that three types of 
neuroblasts may be recognised. For these the names of a, ft, and 
y neuroblasts have been adopted. 

1. The a neuroblasts retain their embryonic character more or 

less. They probably form a reserve of young nerve-cells. 

2. The ft neuroblasts become invested by a very scanty cyto- 

plastic envelope. 

3. The y neuroblasts become transformed into actively func¬ 

tioning nerve-cells. 



It is important to note that nerve-cells begin their life history 
as the a type of neuroblast, and pass successively through the stages 
represented by the /S and y types. 

Several observers, such as Held, Rohde, Holmgren, Scott, etc., 
have shown that the cytoplasm of nerve-cells is rich in nuclein 
compounds. This seems to suggest that a part of it at least is 
derived from the nucleus, as shown in this research. Fragnito and 
Capobianco go so far as to declare that the major portion of the 
adult nerve-cell cytoplasm is derived from the disintegration and 
fusion of the nuclei of ncuroblasts which they style secondary 
neuroblasts, while the nuclei of other neuroblasts (called by them 
primary neuroblasts ) persist as the adult cell-nuclei. 

The nucleus not only gives part origin to the cytoplasm of the 
nerve-cell, but also furnishes a supply of fresh material to replenish 
the latter, when occasion demands, throughout the life history of 
the individual. This function has been clearly demonstrated by 
a study of the effects of fatigue upon the nerve-cells, as investi¬ 
gated by, among others, Hodge, Lambert, Mann, and Vas. The 
nucleus is thus to be regarded as the nutritive centre for the nerve¬ 
cell. As a result of this, it is obvious that a modification in our 
present acceptation of the Wallerian law of nerve degeneration will 
be necessary. The latter would thus come to read somewhat as 
follows: An axon, when cut off from its nutritive centre, i.e. the 
nucleus of a nerve-cell, soon exhibits degenerative changes. 

Author’s Abstract. 

(92) MAN. (Uber Kemteilungen in den Vorderhornsellen des 

Menschen.) Orzechowski, Arb. a. d. neurolog. Instil, a. d. 

Wien. Universitat, Bd. 13, 1906, S. 324. 

Ths author describes and figures certain appearances observed in 
the cells of the anterior horn of the spinal cord after amputation 
of the forearm. The patient (aged 51) whose cord was examined 
died fifteen days after the operation, which was performed on 
account of the presence of tubercle. Before death there was 
slight elevation of temperature. The cord was fixed in formalin. 
The lower cervical and upper two dorsal segments were cut in 
serial section, and the sections stained with thiouin. With the 
exception of the changes in the nerve-cells, little pathological 
alteration had taken place in the spinal cord. On the side of the 
degeneration, all the groups of nerve-cells, except the ventro- 
median, exhibited signs of degeneration. A number of nuclei of 
anterior horn-cells were observed to be in process of division. In 
such dividing nuclei, degenerative changes could frequently be 



seen. Many nerve-cells, including some in which nuclear seg¬ 
mentation could be observed, and others with unchanged anil 
undegenerated nuclei, presented an appearance of complete chro¬ 
matolysis. The author describes the cell changes as post-resective 
appearances complicated by an inflammatory process spreading 
from the seat of amputation along the nerve-sheaths. 

The spinal cord was somewhat flattened in the ventro-dorsal 
diameter, and the majority of the flattened motor cells lay with 
their long axes frontally situated. The nuclear figures, of which 
about forty were observed, are contained almost always in such 
spindle-shaped cells with short ventro-dorsal and long frontal 
diameters. Within these cells the nuclear figures lie with their 
long axes approximately ventro-dorsally placed, forming an acute 
angle with the sagittal line. The appearance presented in most 
cases is that of an elongated, deeply-staining figure, consisting of 
two daughter nuclei united by an intervening bridge of less 
deeply-staining nuclear substance. Around the figure lies a clear 
area which is considered to arise from the fluid part of the nuclear 
substance after solution of the nuclear membrane. In some cases 
the daughter nuclei are well marked off and connected to each 
other merely by threads of nuclear substance, and the process has 
occasionally advanced to almost complete separation of the nuclei. 
A few of the figures appear to indicate division into three 
or four daughter structures. The nuclei frequently contain small 
granules united by fine threads. The presence of degenerative 
changes in the cells raises the question whether the figures 
evidence actual division, or are results of degeneration which 
simulate division. The author considers that degeneration has 
set in in the course of a progressive regenerative process, but that 
the figures do not owe their origin to degeneration. It is possible 
that the structures which are undergoing division are not nuclei 
but nucleoli. Many of the appearances have a superficial resem- 
blance to karyokinesis, but the division which is seen in the 
majority is neither of the direct nor of the indirect type. The 
explanation of this divergence from the recognised forms is to be 
sought in the morphology and chemical constitution of the nuclei 
of the large nerve-cells. 

The author discusses the bearing of his results upon the 
general question of the possibility of proliferation of nerve-cells. 
He has been unable to demonstrate instances of complete separa¬ 
tion of daughter nuclei, but cannot conclude from this that, had 
the spinal cord been examined at a later period, such a condition 
would not have been observed. W. A. Jolly. 




BBADT AND THOUGHT. (Oerveau et pens^e.) Alfred Binkt, 
(93) Arehiv. de Psychol., Aug. 1906, p. 1. 

I. The connection of the brain with thought is the tangled skein 
of every philosophical system. Parallelism is the working hypo¬ 
thesis which dispenses most with the Chinese puzzles of meta¬ 
physics. Its dominant contention is that between the neurological 
phenomena and the mental there exists only a rigorous simul¬ 
taneity in time. But parallelism keeps dangerously near the 
notion of causality, and finally loses itself in materialism. Nor 
are its premises unimpeachable. Berkeley and succeeding idealists 
took the other way of escape, and postulated the purely verbal 
solution of the identity of brain with the objects of perception. 

II. The cardinal difficulty of the discussion consists essentially 
in the irreconcilability between the current produced in the cells 
and fibres of the nervous system and the perceptions l>elonging to 
psychical life. When an external object excites our senses, the 
hang of the mechanism is much the same as the transmission of 
the full blast of an orchestra across a telephone wire with a metal 
diaphragm of a few millimetres in diameter. It is not the sound 
which is propagated along the wire, but its transformation into 
electricity. The size of an object (which is a source of comic 
embarrassment for realists, who want to know how a star aud its 
properties can be brought to heel by a telescope and lodged in the 
brain) is a negligible difficulty when size is taken to mean the 
duration of the excitation, or its intensity, or the number of fibres 
it intersects, or all these qualities at once. Objects are pure 
phantoms created by our imaginations to explain the linkage or 
the genesis of our sensations. Refusal to admit that the little 
brain may contain the great universe is due to making a fetish of 
mechanism. Mechanical continuity is only a symbol, helpful but 

IIL The results of the author’s observations on the relations 
between consciousness and the nervous system are embodied in 
various propositions. 

1. Considered as a physical object, the nervous system is a 
closed and self-sufficing system. 

The brain takes in raw materials and turns out finished goods, 
just like a machine in a factory. Our most poignant joys and 
sorrows are a super-added encumbrance, as useless to the brain as 
to the liver and kidney. 

2. If consciousness, abstracted from what constitutes its object, 
is not a material object, a material phenomenon, a material force, 
nor any constituent whatever of the material world, it is useless to 




seek how contact is made between consciousness and that fragment 
of matter which constitutes the brain. 

Consciousness may be compared to a light bathing the interior 
of the nervous substance, or to an atmosphere in the midst of which 
nervous movements are produced. 

3. The objects we perceive being, as we have seen, of material 
nature (for every sensation is mixed, at once material and mental), 
the relation of these objects with our brain, which is equally of 
material nature, ought to be describable and even observed. 

I see an object: is it this image which is going to act on my 
muscles, or is it the motor current ? If it is the image, the motor 
current is useless. If it is the motor current, where does the 
image come in? 

4. Although the question of the relations between brain and 
thought is the authentic contemporary presentation of an older 
question, that of the connection of the soul and the body, it seems 
evident that this problem is clearly distinct from the problem of 
the correlation of the mental and the physical 

The problems are akin, for the brain is a material body, and 
thought includes what is knowable of the soul. But suppress the 
second problem, you do not get rid of the first. Suppose brain and 
thought to be similar in make-up, both physical or both mental, 
you will have just as much trouble in establishing their interaction. 
Let the pyramidal tract be physical or mental, it is equally difficult 
to explain the action of the will on it. 

5. The whole group of psychical phenomena (sensations, per¬ 
ceptions, ratiocinations, etc.) is localised outside of the nervous 

These emotions and these efforts are the perception of certain 
muscular or visceral states outside the brain. For the man 
ignorant of anatomy the brain has no existence, and the facts of 
conscious life fill the whole cycle of events from excitation to 
response. For all of us at some period of our life the picture of 
the universe is made up of objects perceived plus a series of special 
phenomena like the emotions and the wilL Put the nervous 
system into its proper place and its intercalation makes no differ¬ 
ence in the interpretation. Even the products of the mind com¬ 
muning with itself are essentially excitants of the nervous system. 
Take a recollection. It represents a previous perception ; it is its 
footprint; everything runs on as if the excitant were still active. 
The excitation is renewed twice, that is all. It is none the less 
external to the brain. 

6. The brain conditions and standardises our perceptions. 

Perceived objects which excite a nervous system have need of 

that nervous system, not for their existence, but merely for their 
perceptibility. Just as light does not create the objects it 



illuminates, so consciousness creates neither the brain nor the 
external world. The external world is the finger which is ready 
to press on the button of the electric light apparatus; the 
button and the whole electric installation is the brain; the light 
shoots out and illumines objects which existed before it, and 
could continue to exist after its extinction. The brain is the 
standard, and our perceptions for consciousness only seizes, 
amongst all the knowable properties of an object, those which 
have traversed the nerve. The existence of hallucinations where 
a special state of the nervous system engenders perceptions in 
the absence of a corresponding external object shows that con¬ 
sciousness is shut up in the nervous system. 

7. As the intermediate link in the relations between conscious¬ 
ness and the external object, the brain belongs to the group of 
unknown quantities and not to the group of sensations. 

Appearance must be distinguished from reality. Physiologists 
have shown that the quality of each sensation depends on the 
nature of the nerve excited and not of the stimulant which excites 
it; the optic nerve makes the light response always, whether 
tested by a luminous ray, an electric current, or a blow. There is 
no need to push the induction that light may not exist outside our 
brain ; from the moment that the existence is granted of an inter¬ 
mediate link in the chain of our perceptions, no limit can be placed 
to its possible influence. Appearance is sensation, reality is an 
unknown quantity. Every object can be thought of in two ways: 
as a sensation, or the appearance it assumes in our perceptions; or 
as X the unknown cause of our sensations. These are, as it were, 
two planes, in which the same object can be localised. But it is 
illegitimate to place ourselves in both planes at once. This is 
what we do when we say the brain is the producer of thought. 
The true cause of conscious life is the X brain, unknown and 
inaccessible, whose relations with our thought we cannot seize, 
since we do not perceive it, and know nothing of its structure. 

J. Roy Tannahill. 


(94) NERVE. (Weitere BeitrBge zur Kenntnis der degenerativen 
Neuritis und Atrophia des Htimerven.) Wittmaack, Ztschr. f. 
Ohrenheilk., Bd. 53, H. 1, S 1. 

This paper is a sequel to one formerly published by the same 
author (Bd. 51, S. 161) on experimental degenerative neuritis of 
the auditory nerve, and contains an account of histopathological 



examinations of the organ of hearing in two cases of concomitant 
neuritis due to scarlatina, one of auditory atrophy after typhus, and 
one case of degenerative neuritis in each of the following con¬ 
ditions: senile decay (in a dog), diabetes mellitus, and senile 
cachexia (tuberculosis). Short clinical notes as well as the results 
of the functional examination are given in several of the cases. 

The following conclusions may be drawn from these investiga¬ 
tions: Atrophy of Corti’s organ is secondary to neuritis which 
involves the cochlear nerve, ganglion cells, and nerve filaments; 
pathological changes begin in the periphery of the nerve and reach 
their highest degree in the modiolus cochleae; in severe cases there 
is great increase in the interstitial tissue, but in almost all cases 
there is reduction of nerve bundles and also of cells in the spiral 
ganglion: the latter show crenation of the cell contour, vacuolation 
of protoplasm, disappearance of Nissl’s spindles, and shrinkage of 
the nucleus; the nerve filaments show ampullation of the 
medullary tubes, and, in the later stages, the medullary sheaths 
can no longer be recognised. 

1. In the mildest forms of neuritis Corti’s organ shows shed¬ 
ding and degeneration of isolated hair cells, often combined with 
adhesion of the membrana tectoria to the papilla basilaris; the 
supporting apparatus is well preserved. This condition is seen in 
slow progressive or mild forms of degeneration, and as a rule only 
produces slight degrees of deafness. 

2. The second degree is characterised by the shedding of a 
greater number of hair cells, with slight flattening of the support¬ 
ing apparatus. This change is found in moderately severe acute 
lesions of the nerve. 

3. The most severe degree of involution of Corti’s organ con¬ 
sists in the metamorphosis of the papilla basilaris into an almost 
flat epithelial layer, in which neither the hair cells nor the 
characteristic structure of the supporting apparatus are recognis¬ 
able. This condition has only been found by Wittmaack in the 
most severe and quickly progressing forms of degenerative 
neuritis. In both 2 and 3 the membrana tectoria is atrophic and 
adherent to the papilla basilaris. 

The great difference between the cochlear and vestibular 
branches of the eighth nerve is also prominently shown in these 
researches. In the most severe cases there are only slight changes 
in the end filaments of the vestibular nerve, but never in the stem 
of the nerve or ganglion. This fact is interesting from the point 
of view of the neuron theory, because the nerve end apparatus of 
the vestibular branch never shows secondary involution processes 
analogous to those in Corti’s organ due to neuritis of the cochlear 
nerve. Wittmaack maintains that he has previously proved that 
the cochlear nerve itself can recover, whereas the changes in Corti’s 



organ are permanent. Six plates are appended to the paper show¬ 
ing degenerative changes in the cochlear nerve and the secondary 
involution of Corti’s organ. J. S. Fraser. 


(95) Qebiete dee Nervus Medianns.) Wandel, Deutsche. Ztschr . /. 

NervcnheUk. 1906, p. 436. 

Ik this paper the writer records the features of 11 cases in which 
some type of injury had overtaken the median nerve. In four of 
these, fractures of the arm produced as their chief symptom 
complete paralysis of the thumb muscles (ape-hand) and diminished 
sensibility of the thumb and first three fingers. Five of the cases 
were of the nature of occupation neuroses, aud these the writer 
states affect the median nerve, especially in cigarette-makers, 
ironers, carpenters, users of hammers, and carpet-beaters; in 
most of these there were loss of power in the forearm and hand, 
and sensory disturbances of a painful or anaesthetic nature. In 
the remaining two cases vaso-motor and trophic changes were the 
result of a median neuritis, and involved the skin of the thumb, 
index and middle fingers, and in one case the bones in the terminal 
phalanges of these two fingers. The cases are all described in full 
detail. John D. Comkie. 

(96) sacht durch Creosotum pbosphoricum.) Huet, Neurolog . 

Centralbl., Jan. 16, 1907. 

This paper records seven cases of neuritis of a peculiar type follow¬ 
ing the administration of phosphate of creosote for medicinal 
purposes, which occurred at Haarlem in the autumn of 1905. 
The amount taken varied from 25 to 120 grammes in about two 
weeks, and the symptoms set in about three weeks or more after 
the commencement. 

The chief symptoms were—paralysis of the limbs, involving 
first the legs, later the hands, except in two cases, in which there 
was merely steppage gait; usually reaction of degeneration; loss 
of the Achilles-jerks, but retention of the knee-jerks, except in 
one case; loss of the plantar reflex; atrophy of the calf muscles; 
very slight muscle tenderness ; cold feet, but few other parsesthesire; 
great difficulty in doing fine movements with the hands, such as 
knitting and buttoning. 

Undoubtedly many people had taken the substance who did 



not become affected by neuritis, and the writer thinks that some 
samples may have been impure. Some specimens were tested, but 
found to contain no free phosphorus nor arsenic. The writer dis¬ 
cusses at length the possible rdle of phosphorus, creosote, and 
various impurities as the toxic agent, but does not arrive at any 
definite conclusion as to the substance actually responsible for the 
neuritis. John D. Comrib. 


(97) Cumroe (of Penn.), New York Med. Joum., Oct. 13, 1906. 

It has been more or less conclusively demonstrated by laboratory 
methods that the effects which X-ray exposure has upon the body 
may be classified as electrical, chemical, and inflammatory; chiefly 
the latter. The intima of the blood-vessels shows changes similar 
to those seen in endarteritis, and nutrition is proportionately 
lessened. Sensation in peripheral nerves is destroyed by electrical 
irritation. Prolonged exposure to X-rays produces a hypersemia, 
acting as a counter-irritant. 

Cumroe gives in detail the histories of six cases of neuritis, with 
the effect in each case of repeated X-ray exposures. His con¬ 
clusions are: (a) the X-rays should be employed in neuritis only 
after all other judicious methods of treatment have failed; (6) the 
exposure should be made over wide areas, and frequently repeated; 
(c) the strength of the current and duration of exposure should be 
in direct ratio to the approximate distance of the affected nerve 
structures from the cutaneous surface overlying them: idio¬ 
syncrasies must be considered; ( d ) relief, if obtained, usually 
appears early in the treatment; (e) obstinate cases should be 
treated with a medium tube after apparent cure to assure per¬ 
manency; (/) post-operative treatment in nerve resections is 
highly recommended. C. H. Holmes. 

(98) CORD. (Zwei FSlle von traumatischer Halsmarkaffektion.) 

L. R. Muller and R. Lerchenthal, Deutsche Ztschr. f. 
Nervenheilk., Bd. xxxi., S. 398. 

1. Direct trauma to back of neck. Patient could just walk with 
assistance immediately after. One leg was completely paralysed 
at the end of twenty-four hours, the other not for two days. 
Severe pains occurred in both arms, and after four days in both 
legs as well. After presenting the usual train of symptoms, 



bladder retention, respiratory paralysis, etc., the patient died 
• twelve weeks after the accident. 

The hypothesis did not ever become complete, contrasting 
with the motor phenomena. There was an area of hyperesthesia 
horn the second to the fourth rib, between the hypothesis of the 
eighth cervical above and the total hypothesis below. At the 
autopsy extensive pressure was found affecting the seventh seg¬ 
ment ; this was due to luxation of the sixth vertebra, which, being 
jammed against the fifth, greatly narrowed the canal. The grey 
matter of the cord had almost escaped, and the changes in the 
white matter, which were most marked in the posterior columns, 
were due rather to a sequential myelomalacia than to direct 
destruction. This accounted for the relatively late onset of the 
paralysis. The consecutive changes in the cord are described, the 
amount of ascending degeneration in the comma tract being note¬ 
worthy. The pains in the lower extremities were obviously not of 
root origin, and the author accounts for them by supposing an 
irritation in the leg fibres as they passed through the affected area. 
The upper level of the motor paralysis is fully described, and its 
bearing on localisation. The facts here confirmed the accepted 
teaching on the subject 

2. A powerfully-built man struck his parietal bone against a 
roof and fell unconscious. In the hospital, fifty minutes later, his 
state was as follows: Normal psychically. Pupils greatly con¬ 
tracted, but reacting to light. Arms strongly abducted and flexed 
at all joints (Thorbum's position). They were quite paralysed 
except for flexion of the elbow, and on the left side extension of 
the elbow and radial flexion of the wrist Amesthesia was both 
total and complete below the third rib and along the inner side of 
both arms, and all reflexes were abolished below this level. Marked 
priapism. No local signs in the neck could be detected. Death 
in thirty hours. 

Post-mortem was found a fracture of both laminae of the fifth 
vertebra; its spinous process, though movable, was kept in position 
by the well-developed muscles. Vertical fissure in the body of the 
sixth vertebra. No narrowing of the canal or flattening of the cord 
as in Case 1. No haematorhachis. The cord was normal micro¬ 
scopically down to the middle of the fifth segment. Below this to 
the seventh segment were numerous central haemorrhages The 
axis-cylinders were swollen, but no changes were shown by Marchi’s 

As regards localisation, the case points to the elevators and 
external rotators of the shoulder joint (deltoid, spinati) being 
innervated from the fifth segment, the adductors and internal 
rotators (pectoralis major, latissimus dorsi, and subscapularis) from 
the sixth, the flexors of the forearm (biceps, brachialis anticus, and 



coraco-brachialis) from the fifth, and the extensors from the sixth. 
The pupil changes were due to the centre in the seventh cervical 
and first dorsal segments being cut off. 

Priapism in these cases has been attributed to either an excita¬ 
tion of the fibres concerned or to paralysis of the vasomotor nerves. 
The former is improbable, for it would be the sole evidence of 
excitation present in the midst of extensive paralysis. Bearing 
on its pathogeny are the facts that it is found only in high-seated 
lesions, and that it occurs (in the presence of bitches on heat) in 
dogs, the lower third of whose cord has been extirpated. The 
fibres connecting the brain with the pelvic plexus must thus leave 
the cord at about the mid-dorsal level and perhaps run with the 
splanchnics. Ernest Jones. 

SYRINGOMYELIA IN OLD AGE. (Die Syringomyelia im Senium.) 

(99) K Fries, Arb. a. d. neurolog. Instil, a. d. Wien. Universitdt, Bd. 13, 
1906, S. 170. 

As vascular changes are believed to be an important factor in the 
causation of certain forms of syringomyelia, and as such forms 
would, therefore, be most apt to occur in conditions of weakened 
resistance and pathological changes in the vessel walls, e.g. in old 
age, Fries thinks that too little attention has been paid to the 
study of syringomyelia in old age. There are too few facts to go 
npon to enable one to say whether senile vascular changes stand in 
any relation to the actual origin of syringomyelia; but Fries gives 
full clinical and pathological notes of two cases occurring in 
advanced life, and, on the basis of these and of a few other 
recorded cases, he believes that the following conclusions are 
justified regarding tbe influence of these senile vascular condi¬ 
tions on the clinical course and pathology of syringomyelia 
already existing:— 

1. Syringomyelia occurring in old age differs in no respect as 
regards clinical course from the disease as seen in earlier life. 

2. The pathological anatomy of senile syringomyelia is to a 
certain degree characterised by these two points :— 

(a) The glia-tissue, of which the gliosis consists, completely 
disappears, and is replaced by connective tissue, which arises from 
the adventitia of the vessels —not from the pia mater, as Sterling 

(b) Lateral fissures formed by softening occur, and they need 
not stand in any relation to the central cavity. The area of 
softening may remain as such, or it may be replaced by a sclerosis, 
which again may later break down in consequence of the changes 
in the vessels. 



Thus, senile vascular changes do determine in some degree the 
morbid changes found in advanced life, although the truly syrin¬ 
gomyelic conditions—hydromyelia and gliosis spinalis—differ in 
no respect from the conditions found in earlier life, and are, in 
age as in youth, based on congenital defects of development. 

A. W. Mackintosh. 


(100) my&ie.) Alquier and Lhermitte, Rev. Neurol., Dec. 30, 
1906, p. 1141. 

Clinically what is known as syringomyelic dissociation of sensa¬ 
tion has frequently been remarked in Pott’s disease. Cervical 
spinal caries in particular may present the picture of syringomyelia. 
Pathologically, in the former condition there may exist medullary 
cavities surrounded by a neuroglial wall, independent or not of the 
central canal of the cord. S. A. K. Wilson. 


(101) (Zur Pathologic des Epiconus medullaris.) Minor, Deutsche 
Ztschr. f. Nervenheilk., Bd. 30, p. 395. 

The author has described certain more or less well-defined 
symptoms occurring together in certain lesions of the lower part 
of the spinal cord, and has grouped them clinically. The combination 
of present knee-jerks, intact sphincters, and palsies or anaesthesias 
in the area of the sacral plexus depends on a lesion between the 
second and third sacral roots as a lower limit, and the fourth and 
fifth lumbar as an upper limit. To this section of the cord he 
proposes to apply the term epiconus medullaris. Several instances 
of a lesion of this region are given in detail. The roots which 
leave from the segments involved are included in the term. Thus 
a case of poliomyelitis, in which the knee-jerks are present, but 
the Achilles-jerks absent, the peronei and calf muscles wasted, the 
sphincters intact, and sensibility unimpaired, is a pure case of 
an epiconus affection. A steppage gait is characteristic of the 
condition. S. A. K. Wilson. 


(102) THE CENTRAL NERVOUS SYSTEM. (Em Beitrag zur 
Lehre von den Geschwiilsten des Zentralnervensystems.) W. 

Rosenblath, Deutsche Ztschr. f. Nervenheilk., Bd. xxxi., 
S. 335. 

This article of sixty-two pages is a detailed description of nine cases 
which the author has selected from a series on account of the 
special features they show. 



1. Male, aged 32. Headache, double optic neuritis, double 
exophthalmos more marked on the left side. At autopsy was found 
a tumour, the size of a hen’s egg, at the pole of, the left frontal lobe, 
and implicating the front of the caudate nucleus; microscopically 
it was shown to be a glioma. The orbits were normal. 

There are nineteen cases on record of exophthalmos due to brain 
tumours. They were usually in the frontal lobe, but may be in 
any situation. The symptom has occurred with hydrocephaly and 
cerebral abscess. Flatau’s explanation is that the cause is 
increased pressure occurring in individuals whose orbits are drained 
wholly by the cavernous sinus and not the facial vein. 

2. Male, aged 53. Perfectly well till a fall on to his head five 
weeks before his death. Three weeks later, onset of numerous 
right-sided Jacksonian fits, in which the head and eyes were 
rotated to the right. Paresis of the right limbs, with no spasticity 
or changes in the reflexes. Discs normal. As lumbar puncture 
withdrew blood, late meningeal haemorrhage was diagnosed and 
the patient was trephined. At the autopsy there was a large 
calcified tumour of the left frontal lobe towards its front. The 
Rolandic area was intact. 

The case supports Muller’s and Oppenheim’s teaching that large 
frontal tumours can cause Jacksonian fits by pressure, and that a 
Rolandic lesion can be diagnosed only when the paresis affects 
progressively one limb after another. 

3. Male, aged 43. Quite well till twenty days before death. 
Headache, double optic neuritis, mental symptoms, terminal coma. 
A small glioma was found in the gyrus rectus of the frontal lobe. 
Its recent development provided a good opportunity for the study 
of its structure. This is discussed in great detail. Strobes’ 
hypothesis as to the origin of glioma tissue is controverted. 

4. Male, aged 56. Symptoms for two months before death. 
Paresis and clumsiness of the right arm. Paraphasia. There was 
a fairly large tumour in the left frontal lobe, pressing on the lower 
two frontal convolutions, the island of Reil and the first temporal 
convolution, and reaching to the lower end of the Rolandic fissure. 
It was a glioma with a peculiar plexiform structure. In spite of 
the destruction effected, the patient could speak spontaneously and 
understand all that was said to him. The author discusses the 
difficulty of reconciling the findings with the prevailing views on 

5. Male, aged 22. Symptoms for six months before death. 
Headache, vomiting, optic neuritis, progressive right hemiparesis, 
with no changes in the reflexes. Large tumour in left centrum 
ovale. It was a perithelioma that had undergone cystic degenera¬ 
tion. The relation of rapid formation of large cysts and the 
progress of certain symptoms is pointed out. 



6. Male, aged 36. Headache, apathy, post-neuritic atrophy, no 
localiaing symptoms. Large tumour growing from the arachnoid 
and destroying a great part of the right temporal lobe. It was an 
endothelioma. No metastatic growths were found, as sometimes 
occur. The author examined the growth in vain for normoblasts, 
which have been recorded in such tumours, and have been adduced 
as evidence that they originate in the endothelium of blood¬ 

7. Male, aged 43. Slight left hemiparesis, especially in the 
arm. Ataxy, asymboly, astereognosis, and tremor of the left arm. 
Papillitis developed late, with fixed pupils. The tumour was an 
endothelioma growing over the light parietal lobe and extending 
to the upper and back part of the frontal. It was therefore too 
huge to be of any value in the localisation of the cause of the 
asymboly (Tastlahmung), though it supports Wernicke’s view that 
this is cortical. The Argyll-Robertson pupil was inexplicable in 
the case. 

8. Male, aged 49. Symptoms for only six weeks. Sudden 
onset of left brachial monoplegia, followed in a few days by para¬ 
lysis of the leg also. This became complete, but sensation remained 
intact. A month later it was noticed that there was complete left¬ 
sided respiratory paralysis; not a sound could be heard in the chest 
on that side. The tumour was situated on the medulla, and affected 
the pyramidal tract just below its decussation. It grew from the 
pia between the cerebellum and medulla. In structure it was a 
spindle-cell sarcoma, the cells and tissues of which were impreg¬ 
nated with pigment. No primary melanotic growth was to be 
found. The respiratory paralysis is explained by the author as 
being due to pressure on the upper cervical cord of that side. 

9. Male, aged 22. Headache, apathy, optic neuritis, spinal 
tenderness. Slight paralysis in the left arm, complete in both 
legs. Knee-jerks present. Plantar reflexes and left Achilles-jerk 
absent. Anaesthesia below the fourth rib. There was diffuse 
tumour infiltration of the whole length of the cord and extensively 
at the base of the skull, implicating both temporal lobes and the 
cerebellum. Microscopically it was an alveolar round-cell sarcoma, 
though its structure varied much in different localities. 

Ernest Jones. 

(103) CEREBRUM. Charles K. Mills, M.D., Univ. of Penn. Med. 

Bull., April-May 1906. 

The scope of this paper is limited to a discussion of the focal 
diagnosis of operable tumours of the cerebrum. By operable, Dr 
Mills implies tumours situated so as to be accessible to the surgeon. 



Further, this paper is in large part a summary of many previous 
publications which the author 1ms made on cerebral localisation, 
and as such necessarily lacks much of the detail and evidence 
upon which his conclusions have been based. The author briefly 
describes the general symptoms of intracranial neoplasms, without 
entering at all fully into their localising value. He divides the 
brain into the frontal, parietal, occipital, and temporal regions, and 
for the purpose of diagnostic study subdivides these areas into the 
following six regions according to their physiological functions: 
(1) pre-frontal or higher psychic, (2) mid-frontal or intermediate 
psychic-motor, (3) post-frontal or motor, (4) parietal or sensori- 
stereognostic, (5) parieto-temporal or visuo-auditory, (6) occipital 
or visual. Before entering into the description of tumours of 
these various areas, he calls attention to the preponderating part 
played by the left hemisphere in the faculty of speech, and ex¬ 
presses the opinion that the cortical representation of cutaneous 
sensibility, muscular sense, and stereognosis has a higher evolution 
in the left hemisphere than in the right. 

Pre-frontal or Higher Psychic Region is that part of the 
frontal lobes which lies anterior to a line drawn vertically to the 
mesial surface from a point half an inch in front of the anterior 
branch of the Sylvian fissure. Dr Mills recognises that much con¬ 
fusion has ariseu regarding the functions of this region, owing to 
the misinterpretation of the mental symptoms due to intracranial 
tumour in any situation, and the failure to distinguish between 
those due to increased intracranial pressure and those resulting 
directly from involvement of the pre-frontal region. One regrets 
that with the recognition of this difficulty the author did not 
devote more space to its elucidation, in place of entering rather 
fully into indirect and distant symptoms due to lesions in other 
parts of the brain. The psychic changes characteristic of pre¬ 
frontal lesions are described as “evidences of higher psychic 
dissolution, which is shown in loss of memory and of powers of 
attention, abstract conception, comparison, judgment, and higher 
imagination.” Beyond stating that tumours of the orbital surface 
of the frontal lobe give rise to psychic, olfactory, and optic tract 
symptoms, and that the psychic symptoms are probably more 
marked in lesions of the left pre-frontal region, there is no attempt 
to help one to localise a tumour of the right or left side. Excep¬ 
tion must be taken to the statement that in order that any 
decided effect upon the mentality of the individual shall result, the 
lesion of the pre-frontal lobe must be destructive, and that charac¬ 
teristic mental changes do not occur without such destruction 
having taken place. This statement is too sweeping, and cannot 
be justified by clinical experience. 

Mid-frontal or Intei'inediate Psychic-motor. —This area, which lies 



behind the pre-frontal and in front of the ascending frontal con¬ 
volution (post-frontal region), contains the graphic centre in the 
posterior part of the 2nd frontal convolution, the speech centre in 
the posterior part of the 3rd frontal convolution, and centres for 
the movements of the head and eyes intermediate between them. 
The symptoms of tumour of this region (on the left side) are tem¬ 
porary or permanent motor aphasia with Jacksonian attacks; 
Jacksonian epilepsy, affecting head, eyes, face, hand, and upper 
extremity; and some psychic changes. Destruction of the graphic 
centre alone results in inability to use the hand tor graphic pur¬ 
poses, although full power of movement is retained. Tumours of 
Broca’s convolution cause motor aphasia, sometimes recurring 
utterance, but no agraphia. Tumours growing from the mem¬ 
branes are characterised by an irregular development of agraphia 
or aphasia, and function is retained longer than in subcortical 
lesions. The importance of studying the initial and invasion 
symptoms is well brought out. 

Post-frontal or Motor .—The localisation of such tumours is easy, 
the distinction between cortical and subcortical being based upon 
the frequent spasm and slighter spasticity in the former, and the 
rarer spasm and greater spasticity in the latter. The observations 
upon the conditions giving rise to Jacksonian epilepsy will be 
agreed to by all. 

Parietal or Sensori-stereognostic .—This area is bounded in 
front by the fissure of Rolando, below by the fissure of Sylvius, 
and behind by a line drawn from the parieto-occipital fissure to 
the posterior end of the fissure of Sylvius. Cutaneous sensibility 
is represented in the post-central gyrus; muscular sensibility 
in the anterior portions of the superior and inferior parietal con¬ 
volutions and stereognosis in the posterior part of the superior 
parietal. Cutaneous representation is apart from that of move¬ 
ment, and there are distinct areas for the sensory representation of 
the face, arm, leg, trunk, etc. Further, the author thinks that 
special areas of skm are definitely correlated with subdivisions of 
the sensorial and stereognostic cortex, and that the restricted 
centres and subcentres for sensation and stereognosis are cor¬ 
related anatomically and functionally with special cortical motor 

Stereognosis is a conceptual process brought about by the 
recalling of memorial images obtained through such senses as 
contact, pain, temperature, location, vision, etc. There is no 
definition given of what is meant by muscular sensation or 
sensibility. The positive focal symptoms of a cortical parietal 
tumour are moderate impairment of cutaneous sensation, especially 
of pain and temperature sense, diminution of muscular sensibility, 
and stereognosis. Motor or visual affections occur if the growth 



spreads respectively anteriorly or posteriorly. An absence of the 
plantar reflex and a diminution of the corresponding deep reflexes 
is referred to as characteristic of a strictly limited parietal tumour, 
but both these signs are met with in tumours situated elsewhere 
in the brain. In subcortical tumours the sensory symptoms are 
more complete. One wishes that more had been said about the 
paralytic negative and irritative positive symptoms of lesions of 
this area. 

Region of the Junction of the Temporal, Parietal , and Occipital 
Lobes. —Tumours of this region on the left side affect the highest 
visuo-auditory centres, and word-blindness, word-deafness, reading, 
etc., hemianopsia or astereognosis if the tumour spreads forwards 
or backwards. 

Middle Temporal and Inferior Temporal. —As the author 
leaves out of consideration the uncinate and hippocampal regions, 
and any reference to dreamy states, there is nothing special to 
guide one in localising a growth of this region. 

Occipital or Visual Area. —A tumour on the external surface 
of the left occipital region causes visual aphasic symptoms, 
hemianopia, or perhaps astereognosis. If situated on the right hemi¬ 
sphere the aphasic symptoms are wanting. 

The author concludes by some remarks on the sources of error 
in the focal diagnosis of brain tumour, and largely follows the lines 
of Collier’s paper on the same subject. The paper finishes with 
a short and incomplete reference to the symptoms caused by deep- 
seated tumours. T. Grainger Stewart. 


(104) G. E. DE Schweinitz, Univ. of Penn. Med. Bull., April-May 1906. 

The name of this article is misleading, as the author confines 
himself to describing the papillitis and retinal changes, and to a 
brief reference to visual field phenomena. Although no new 
points are brought out in the paper, the author is in general agree¬ 
ment with most of Paton’s observations on the effect of operation 
on the optic neuritis. T. Grainger Stewart. 


(105) BY OPERATION. (Ein operativgeheilter Tumor des Occi- 
pitallappens des Oehims.) Oppenheim and Krause, Berl. 
klin. JPchnschr., Dec. 17, 1906. 

This paper records the symptoms and removal, with singular 
success, of a tumour from the left occipital pole of the brain. The 
symptoms and signs presented were, in brief, headache, giddiness. 



vomiting, double optic neuritis especially marked, and associated 
with retinal haemorrhages on the right side; later, left-sided 
hemianopsia; and still later, difficulty in writing and reading, 
with right-sided hemiataxia, hemiparesis, and hemihypaesthesia. 
The various anti-syphilitic remedies having been tried without 
benefit, the left occipital region was trephined, and a large tumour 
found adherent to the dura mater, occupying the posterior extremity 
of the right occipital lobe, and extending down its mesial surface 
to the cuneus. This tumour was of the size and shape of a large 
hen’s egg, shelled out easily, and proved to be a spindle-celled 
sarcoma. The adherent piece of dura mater was also removed. 
The wound healed well and a good recovery resulted. At first 
the patient had some visual hallucinations, seeing coloured patterns 
before the eyes, halos round objects, and an appearance of convexity 
or concavity in everything he looked at. A fortnight after the 
operation the optic neuritis had much subsided, and a week later 
the hemianopsia had largely disappeared. Within six months the 
patient was in the full activity of his business once again. Illus¬ 
trations are given of the tumour and of the operation. 

John D. Combie. 

(106) Epilepsie bei Ohren- und Nasenkrankungen.) Hugo Frey 
and Alfred Fuchs, Arb. a. d. neurolog. Instil, a. d. Wien. 
Universital, 1906, Bd. xiii., S. 78. 

This was an opening paper read at the Oto-Rhinological Section 
of the Lisbon Congress, 1906. The authors divide the Epilepsies 
into three groups—Jacksonian, Symptomatic (unemia, Stokes- 
Adams, etc.), and General. Ninety-two cases were collected from 
the literature: 42 concerned ear affections, 16 being chronic sup¬ 
puration, 41 concerned nose affections, 18 being chronic rhinitis 
with hypertrophied turbinates. The majority of these cases do 
not, however, teach us anything, because of the incompleteness of 
the description. The authors have examined 112 personal cases 
of epilepsy, and found ear, throat, or nose affections in 30; these 
were all treated locally. Sixteen had no other treatment, and four 
of these showed improvement of the epilepsy as a result. The cases 
were observed for a year only. 

Mequius had shown that dogs suffering from repeated epilepti¬ 
form attacks as a result of nasal infection with mites were cured 
by antiparasitic treatment. Brown Sequard’s well-known guinea- 
pig experiments are also referred to. 

The author’s conclusions are: (1) In children suffering from 
epilepsy, or predisposed to epilepsy as a resiflt of infantile cerebral 
disease, chronic poisoning, head trauma, etc., it is probable that 



diseases and foreign bodies in the ear, nose, or throat may evoke 
epileptic attacks in the same reflex way as other peripheral stimu¬ 
lation. (2) In such cases local treatment may remove one of the 
exciting factors of the attacks. (3) It is not justifiable to speak of 
the epilepsy being cured thus, as only the exciting focus is removed, 
the predisposition remaining. (4) It is possible that the local 
affections cited may be more important excitants of epileptic 
attacks than peripheral excitation elsewhere. (5) Epileptics 
should be examined and treated from this point of view. 

Ernest Jones. 



mal avec aure paramn&ique; illusion de fausse reconnaissance.) 

Seglas, Rev. Neurol ., Jan. 15, 1907, p. 1. 

The patient was a man aged 28, who for four yeai*s had suffered 
from peculiar psychical troubles. At certain times he suddenly 
felt that he had been in exactly the same situation before. The 
environment, the people, their gestures and words, his own 
thoughts, all appeared to constitute a scene through which he 
had been before, though it was in reality quite new. Sometimes 
this feeling came over him as he was falling asleep; it was often 
called into being by emotion, or by intellectual or physical fatigue. 
He had also remarked the appearance of these paramnesic attacks 
if he came to a sudden halt after walking briskly. The duration 
of the sensation was merely a few seconds. At other times, 
however, it was the prelude of a more complex syndrome. No 
sooner had the feeling arisen, than he felt as though he were 
going to choke; his face became pale and his eyes fixed. Ques¬ 
tions addressed to him were unheeded. Sometimes he remained 
still; sometimes he moved aimlessly about, muttering incoherently. 
After some minutes he usually recovered and continued what he 
had been doing previously, but he was always more or less 
completely ignorant of what had just taken place. The sensation 
was not infrequently associated with a feeling of anxiety or 

It seems clear enough that, the false recollection apart, the 
other phenomena were of the nature of petit mal. and the sensation 
itself may be regarded as a sort of aura. The case resembles one 
published by Hughlings Jackson, where an epileptic suffered from 
fits, the aura of which was this sensation, and from petit mal with 
an identical aura, followed by complete amnesia both of the fit 
and of the aura. S. A. K. Wilson. 



09 FREQUENT PETIT MAL ATTACKS. (Ubn gsUofto klslns 
(108) Anfllle.) Karl Heilbronner, Deutsche Zeitschr.f. NervenheUk., 
Bd. xxxi., S. 472. 

The author looks upon hysteria as a functional disease in the 
sense that we cannot expect ever to find anatomical changes 
underlying it, for its manifestations are throughout psychical; 
whereas epilepsy is a functional disease in the sense that though 
up to the present no characteristic changes are kuown, we may 
expect, with further perfection of technique, some day to discover 
them. The two diseases are thus theoretically separable, however 
much they may appear clinically to fade into each other. The 
great difficulty of diagnosing hysterical attacks from epileptic, so 
far from diminishing with our increased knowledge of the con¬ 
ditions, has considerably increased, chiefly owing to the recognition 
that more phenomena are possible in hysteria than was previously 
conceived. In fact at present the state of affairs is such that 
though in many cases we can say that a given attack is certainly 
hysterical in nature, it is hardly ever possible to say that any given 
attack is certainly epileptic. In other words, diagnosis of hysteria 
is always more sure than its exclusion. Especially is this so in the 
case of “ minor attacks ” due to hysteria, which may in all points 
be quite indistinguishable from minor epilepsy. Thus the diag¬ 
nosis of minor epilepsy can only be made in the absence of other 
evidences of hysteria, and even then only tentatively as a rule. 
Although the above conclusions have been fully established, it is 
surprising how little known are the facts concerning hysteria on 
which they are based. 

In this monograph of forty pages the author confines himself 
almost exclusively to the “nicht epileptischen Absencen ” that 
Friedmann treated recently (see Review of Neurology, 1906, p. 575), 
and considered to # be identical with Gdlineau’s narcolepsy; he dis¬ 
cusses only those cases that occur in children. The varying 
symptomatology is given in detail, with numerous illustrative 
cases. Heilbronner agrees with Friedmann that most of the cases 
are not epileptic in nature, but is very sceptical about the attempt 
to establish narcolepsy as an entity quite distinct from other 
functional conditions. His main argument, which he repeatedly 
emphasises from various points of view, against the epileptic nature 
of the cases, is that they show no tendency, even after many years, 
to manifest intellectual decadence. He allows that there is a certain 
group of epileptics of whom also this is true, but outside this well- 
defined group he is unwilling to admit the epileptic nature of any 
attacks, repeated many times, that do not cause any psychical 
degeneration. He agrees fully with Binswanger that the epileptics 
who show this degeneration with the greatest certainty are those 




occurring in childhood, and suffering from numerous abortive 
attacks, so that were the cases in question epileptic they would be 
just the cases to show mental changes. He does not lay the stress 
that Friedmann does on the loss of consciousness that occurs in 
petit mal, contrasting with the clouding that is found in narco¬ 
lepsy; the variations in the depth of unconsciousness in petit 
mal are so great, as is the difficulty of estimating its depth in a 
short attack in a child, that, in our present knowledge, the point is 
of little value. The extraordinary number of attacks that may 
occur, even up to a couple of thousand in a day, and the sudden 
or rapid onset of the condition, are two points strongly favouring 
its functional origin. The condition may be simulated by several 
others, notably the attacks in juvenile G.P.I. and Jacksonian 
epilepsy. Its relation to reflex epilepsy is also discussed. 

In conclusion, although Heilbronner maintains that these 
cases are true functional states and not of organic origin, which 
for him is the important problem to decide, he is less certain as to 
their exact position. He cannot accept narcolepsy as a separate 
entity for reasons indicated above, and because writers on the 
subject do not agree as to what are the important distinguishing 
features of what they term narcolepsy; he inclines towards in¬ 
cluding it under hysteria. The absence of other signs of hysteria 
does not exclude this diagnosis—a point on which Binswanger 
also insists—for monosymptomatic hysteria is a well-recognised 
condition, and especially frequent in children. 

Ernest Jones. 

(109) CHILDHOOD. James M'Ilraith, The Medical Chronicle , 
Nov. and Dec. 1906 and Jan: 1907. 

At the close of his somewhat intricate and unduly detailed paper, 
founded on the study of 250 cases, the author arrives at the follow¬ 
ing conclusions, which I state in full:— 

1. Convulsions are most frequent during the first year of life, 
and not very frequent after the third year. 

2. The predisposing are more important than the exciting 

3. The predisposing causes are “ an inherited neurotic taint ” 
and rickets. 

4. Healthy children born of healthy parents rarely suffer from 

5. In children suffering from convulsions there is frequently 
a history of ill-health or disease in the parents, especially in the 
mother during pregnancy, and this acts by lowering the vitality of 
the child and rendering it more liable to disease. 



6. The family history of children suffering from convulsions is 
bad. Frequently the brothers and sisters suffer, and the mortality 
in these families is high. 

7. Only a small proportion of cases can be ascribed to organic 
disease of the brain. 

8. Only a small proportion of cases of convulsions can be 
ascribed to injury at birth. 

9. The most common cause of convulsions in the first two 
months of life is reflex irritation from the alimentary tract. 

10. The great majority of convulsions are due to reflex causes. 

11. Dentition is rarely a cause of convulsions, and only when 
some predisposing cause exists. 

12. Gastro-intestinal disorders are the chief exciting causes of 

13. Convulsions are by no means as frequentas generally supposed 
at the onset of acute fevers, such as measles and pneumonia. They 
are more common at the onset of pneumonia than at the onset of 
measles. When they do occur there is usually some predisposing 
cause present. 

14 In several of the cases of convulsions associated with 
whooping-cough a predisposing cause is present. Convulsions are 
by no means frequent in whooping-cough when no predisposing 
canse exists and no complications occur. 

15. Convulsions in early life may be the first sign of epilepsy, 
or may give rise to that condition in later life, and are more 
likely to become epileptic when there is no obvious cause for the 

16. The fundamental cause of convulsions is some predisposing 

cause. A. Dingwall Fordyck. 

H7BTERIA IN CHILDHOOD. (Ueber Hysteria bei Kindern.) 
(110) Rudolf Fischl, Prag. med. Woch., Nos. 51 and 52, 1906. 

Ix his article on this subject the author states that the earliest age 
at which the condition is met with is towards the end of the second 
year of life, and then only rarely. 

In the fourth and fifth years the disease is by no means rare, 
and increases in frequency from this time onwards till puberty. 
From puberty onwards, sex differences are noticeable in the fre¬ 
quency of the disease, it being considerably more common in girls 
than boys. 

Its occurrence throughout childhood generally must, however, 
be considered relatively uncommon; and, while heredity and 
environment appear to play little part in its development, con¬ 
tinuous school work is undoubtedly an important factor in its 



It has been customary to consider the great characteristic of 
the disease in childhood its mono-symptomatic nature. The cor¬ 
rectness of this view the author questions. Common symptoms 
are the tdche ciribrale and increased tendon reflexes. The relation 
of the disease to “ Spasmophilie ” and their connection with the 
absorption of calcium salts is considered, and the author takes up 
the position that probably many cases of hysteria occurring in the 
later years of childhood owe their origin to a previous condition of 
“ Spasmophilie.” 

In the experience of the author, the disease occurs in relatively 
simple and slight forms, and does not, as a rule, simulate any 
serious disease. 

That it is, however, a disease per se, he insists upon, and as a 
disease it must be carefully treated. The commonest symptoms 
are cough, recurring vomiting with acetonuria, “ school headache ” 
—more especially during the study of German syntax!—unilateral 
blepharospasm, and joint neuralgia. 

Early diagnosis of the condition is important, and the prognosis 
is relatively good. 

In the treatment, suggestion, moral suasion, alteration of en¬ 
vironment and conditions of life are the essential elements. In 
some cases it is necessary to have resort to various other methods 
—unpalatable or strong-smelling medicines, laryngoscopic exami¬ 
nation, faradisation, and so forth. 

A. Dingwall Fordyce. 

AMBULATOR? AUTOMATISM. (Automatisms ambulatoire.) Paul 
(111) Courbon, Ann. Mid.-Psych ., Jan.-Feb. 1907, p. 22. 

This is a full clinical record of five patients presenting the 
symptom of ambulatory automatism, in each of whom the condi¬ 
tion was attributable to a different cause. In the first case the 
attacks were periodic, and their first appearance had been coinci¬ 
dent with the cessation of malarial seizures, from which the 
patient had previously suffered. They were probably of a hysteri¬ 
cal nature, although events occurring during an attack were 
remembered subsequently. The second was a good example of 
hysterical somnambulism, the incidents of the excursions leaving 
no trace in the memory. The patient was also subject to attacks 
of petit mal. In the third patient the attacks came on as a direct 
result of terrifying hallucinations caused by alcoholism, in marked 
contrast to the first two cases, where the expeditions were quite 
irrational and purposeless and seemed to be compelled by some 
mysterious and irresistible force. The fourth case, one of dementia 
praecox, illustrated an entirely different variety of the condition. 
The attacks were simply manifestations of the dementia, and had 



no origin specially different from the other symptoms of the disease. 
The last patient was a soldier in whom the attacks took the form 
of repeated desertions. Although a man of inferior mental 
development, he could not be placed in the same class os the pre¬ 
ceding patient, because his psychical condition showed no signs 
of progressive deterioration. He was regarded as being the subject 
of constitutional instability, and was not held fully responsible for 
his actions. Henry J. Dunbar. 

(112) NEURASTHENICS. (Ueber auffaUende Resnltate der 
Blutuntersuchung bei NervSsen.) Goett, Muench. mtd. 
fPchnschr., Nov. 20, 1906. 

The writer records the cases and results of blood examination in 
four cases of young men with marked neurasthenic symptoms, 
who all presented the peculiarity of a good haemoglobin percentage 
with a great diminution of the red corpuscles. The figures were 
82 with 3J millions, 100 with 3£ millions, 90 with millions, 
and 95 with 2£ millions. The writer discusses the cause of this 
peculiarity, and gives a bibliography of articles bearing on the 
subject. John D. Combie. 

(113) Unfallneurosen heilbar ?) DOllken, Neurolog. Centralbl., Dec. 1, 
1906, Jahrg. xxv., S. 1099. 

This paper, which is based on a very extensive experience, was 
read before a meeting of the Mid-German Psychiatrists and Neuro¬ 
logists. The writer first discusses some of the etiological factors, 
operations during labour, injuries during games and trade pursuits. 
As there is no form of injury that will fatally induce neurosis, 
other factors must exist. Of these the author discredits heredity 
almost entirely; alcoholism is also unimportant. The prognosis 
and treatment of chronic neuroses incurred during trade pursuits 
are so special as almost to make this a disease apart. The writer 
has in the past eighteen years attended 13,000 workpeople, in 
four factories. He has demonstrated that when full wages are 
paid during the incapacitation of a workman, the acute traumatic 
neuroses, which are fairly common, hardly ever become chronic. 
On this, and on the skill of the doctor who first treats the case, 
argely depends the prognoBia It is almost impossible to give an 
accurate prognosis on the nature of the symptoms alone. The 
writer’s conclusion on this point is strongly that both the existence 



and the incurability of chronic neuroses are due to social condi¬ 
tions, which explains why medicine has failed so manifestly in 
their treatment. “ Soziale tTbelstande und ihre Folgen lassen sich 
nicht mit Medikamenten und Elektrisieren aus der Welt schaffen.” 
The rest of the article is taken up with a discussion of these social 
conditions and their remedies. Ernest Jones. 

MIGRAINIO PSYCHOSES. A. Gordon (of Philadelphia), Joum. 

(114) Am. Med. Ass., Jan. 5, 1907. 

The author reports twelve cases which he has seen during the 
past four years, in whom fairly typical psychoses were observed 
during migrainic attacks. In the majority of these cases the 
mental symptoms developed at the time when the headache had 
reached its climax and disappeared with the headache. The 
mental symptoms which he has found to be invariably present are 
confusion, mild stupor, hallucinations (mostly visual), unsystema¬ 
tised delusions, and delirium. Illusions of identity, incoherence 
of language and thought, and disturbance of orientation have been 
observed. He believes that a certain group of cases may be of an 
epileptic nature; the cause of the migrainic attacks and of the 
psychoses is commonly the same, i.e. auto-intoxication. Constipa¬ 
tion, obesity, defective heredity are the most common antecedents. 

C. H. Holmes. 

AUTO-SUGGESTION AND SEA-SI0ENES8. (Influence de l’auto- 
(115) suggestion sur le mal de mer.) H. Zbinden, Archiv. de 
Psychol., Aug. 1906, p. 153. 

A friend of Dr Zbinden, with no previous sea experience, engaged 
himself as ship’s surgeon on a voyage from Hamburg to Chili. 
The ship was due to sail during the night, and at two o’clock the 
surgeon was awakened by noises as of a ship on its course, and was 
seized with severe vomiting. In reality the ship was still in port, 
and the noises were due to the loading up of cargo. Shame at his 
impressionability cured the surgeon of the tendency to nausea, 
and he made the voyage without mishap. Following out the hint, 
Dr Zbinden made observations on himself and his fellow passengers 
during a rough passage of three days from Norway to England. 
By repeating to himself that he would not be sick, walking about 
(to a polka step), eating and smoking freely, and generally com¬ 
porting himself like the old sea-dogs on board, he succeeded in 
being the only passenger unaftlicted. Some experimental sugges¬ 
tions he made to fellow-passengers met with success. He remarks 



that the mere fact of seeing somebody sick may have on other 
people a suggestive influence analogous to that of a nervous tic, 
which may contaminate a whole form at school. To guide check 
experiments, he sums up his attitude as follows:— 

1. Sea-sickness is in all probability a neurosis. 

2. It can be provoked or inhibited by auto-suggestion. 

3. The fact of distracting the patient’s attention from his woes 
assists the cure as in other neuroses. 

J. Roy Tannahill. 

(116) AFTER TRAUMA (Ueber periodische transltorische 

Bewusstseinsstdrnngen, Dipsomania, u.s.w., nach Trauma.) 

Artur Pelz, Monatsschr. f. Psyckiat. u. Neurol., Jan. 

1907, Bd. xxi., S. 53. 

Under the title of “Mental Symptoms after Trauma” have 
been described the most diverse phenomena, so that it would 
appear almost as if any group of symptoms may thus originate. 
Attempts have been made to separate off precise syndromes that 
could be characteristic of traumatic neuroses. The present article 
is such an attempt. 

Post-traumatic periodic disturbances of consciousness almost 
always develop on a basis of hysteria, neurasthenia, epilepsy, or 
alcoholism. The author critically reviews a number of published 
cases, and concludes that only one of them comes, not into this 
group, but into the section he now tries to establish. On the basis 
of three personal cases he fully describes, he maintains two prin¬ 
cipal theses: first, that there exists a group of periodic attacks of 
twilight states (Dammerzustande) occurring after trauma, and apart 
from any basis such as those mentioned above; and secondly, that 
typical dipsomania, having no relation to epilepsy, may thus 

The first case, which is the most striking, runs shortly as 
follows: The patient, a man of 48, was run over by a train fourteen 
years ago, and had to have his right foot amputated in consequence. 
After this he suffered from many symptoms of psychosis, such as 
giddiness, headache, anaesthesia of the right cheek, etc. Four 
years ago his condition became worse, especially as regards the 
intolerance for alcohol that he had manifested since the accident. 
The following phenomena then occurred. For many months at a 
time he would be a steady, abstinent, regular workman, good- 
natured and peaceful, and a particularly fond husband and father. 
Then gradually would develop loss of sleep and appetite, great 
increase of sexual desire, marked excitability, restlessness, and 



irritability. This phase would culminate in an irresistible impulse 
to drink, all his belongings would be sold, until after lying coma¬ 
tose in the gutter he would be brought home by the police. He 
then would tear his clothing, fling his children out of bed, threaten 
to strangle them and his wife, and violently accuse the latter of 
infidelity. After coming round he would spend a couple of days 
weeping, imploring Ins wife for forgiveness, vowing abstinence, 
etc. This would be followed by almost complete amnesia for the 
whole incident, and some months of perfect behaviour, during 
which time he would have a strong distaste for alcohol. 

The later stage of the condition was thus certainly a dipso¬ 
mania. Atypical features were the sexual excitability before the 
attack, which is unusual in dipsomania, though not unknown ; the 
large quantity of alcohol consumed in the attack—the dipsomaniac 
is frequently satisfied without producing marked physical results 
of intoxication; and the jealousy delusions, which in true dipso¬ 
mania follow the attack, and are not co-existent with an abrupt 
crisis, as in the present case. There was no hereditary taint and 
no history of previous heavy drinking, both significant features. 
The author next discusses the accepted view of Kraepelin, Bin- 
swanger, etc., that dipsomania is always a manifestation of epilepsy. 
He dissents from this opinion. In the above case there was not 
the slightest indication of epilepsy in the present or past condition 
of the patient. Traumatic epilepsy hardly ever occurs except after 
head injuries. Traumatic reflex epilepsy can likewise be excluded, 
as the scar gave rise to no symptoms. Wagner has published a 
similar case of dipsomania occurring after trauma. 

In the three cases here described no attempt was made, 
by Freud’s treatment or otherwise, to probe the disaggregated 
focus of mental content that must have existed, so that the value 
of the observations and conclusions drawn therefrom is relatively 
slight. Ernest Jones. 

(117) Kasuistik der tonischen Kr&mpfe des Rumpfes.) Fuchs, 
Wien. ldin. Wchnschr ., Nov. 29, 1906. 

The writer gives the details of the case of a woman, aged 35, who, 
apparently as the result of a fall upon the back during pregnancy, 
suffers from a condition of extreme lordosis (12£ cm.) with cervico- 
dorsal kyphosis. The head also hangs forwards upon the chest, 
and walking is almost impossible. The condition is not always 
present, as she can at will straighten her back ; but after a few 
seconds, whether she be standing or lying, the deformity gradually 
comes on. As it appears, the erector spinae stands out more 



evidently. An X-ray photograph as well as gynaecological and 
surgical examination discovered nothing abnormal. The writer 
attributes the condition to a functional spasmodic contraction of 
the erectores spinae, and compares it to the condition frequently 
met with in the neck. John D. Comrie. 


(118) SON PHENOMENON. (Zur prognostischen Bedeutung des 
Argyll-Robertson’schen Ph&nomens.) Alexander Pilcz, 
Monatsschr. /. Psychiat. u. Neurol ., Jan. 1907, Bd. xxi., S. 46. 

It is only ten years since Karplus dared to challenge the dogma 
that pupil fixation was diagnostic of epileptic as opposed to 
hysteric convulsive attacks. Since then its occurrence in the latter 
has been fully proved by Oppenheim, Westphal, etc. Marked 
aniscoria certainly may occur in neurasthenia, as for instance in 
eleven of Peligaeus’ 320 cases ; this also has been confirmed by 
Krafft-Ebing and many others. A feature of neurasthenic aniscoria 
is its variability, sometimes one pupil, sometimes the other being 
the larger. 

The author now raises the question as to whether the Argyll- 
Robertson pupil is such certain evidence of organic disease as it is 
generally assumed to be. It undoubtedly is not pathognomonic 
of parasyphilis. Syphilis may give rise to it without there being 
any other affection of the nervous system manifest. The sign may 
occur also in the periodic psychoses, in paranoia, dementia praecox, 
etc. The literature on the subject is referred to extensively. 
Seven cases of psycho-neurosis are then described, in which various 
pupil changes, particularly sluggishness to light, were present. 
The cases were carefully observed for some years. Three of them 
the author selects as being particularly significant; in one of these 
the light reaction was quite lost, in the other two it was very 
sluggish. He does not definitely commit himself to the view that 
the phenomenon was due to the neurosis, but speculates as to 
this possibility. Speaking of the patients with psychical symp¬ 
toms that are diagnosed as cases of general paralysis on the sole 
confirmatory evidence of the Argyll-Kobertson sign, he urges that 
they should be looked at more sceptically from the point of view 
he indicates, and that lumbar puncture Bhould invariably be 
performed. Ernest Jones. 


(119) masticateurs dans rhdmipldgie.) Miralli£ and Gendron, 
Rev. Neurol ., Dec. 30, 1906, p. 1145. 

In fourteen cases of hemiplegia examined specially as to the 
condition of the muscles of mastication, it was found that the 



temporals contracted equally while the masse ters did not, or that 
lateral movements were defective, or that the inferior maxilla 
could not be pushed forward without its deviating to one side, or 
that diduction was impossible. The graver and the more recent 
the hemiplegia, the more noticeable were the defects. 

S A. K. Wilson. 

(120) das Verhalten einiger Reflexe im Schlaf.) Kutner, Deutsche 
med. Wchnschr., Jan. 17, 1907, p. 98. 

Kutneu’s researches were made on male patients at the Breslau 
lunatic asylum. The knee- and ankle-jerks and plantar reflex 
were investigated. In all the cases the examination was repeated 
on the following morning, when the patients were awake, and, as 
far as possible, in the same position. The knee-jerks were examined 
in twelve cases, the ankle-jerks in twenty-two. The knee-jerks were 
present in all. In three cases the ankle-jerks were absent, but they 
were also absent in the waking condition, except when the patient 
was placed in a different position from that assumed in sleep. 
Kutner is therefore sceptical as to the diminution of the tendon- 
jerks alleged by some authors to occur in sleep. Such results he 
attributes to the difliculty of the technique. Only certain positions 
are available without waking the patient, and even in deep sleep 
complete relaxation of the joints, especially of the knees and ankles, 
is not always realised. 

There was no difference between the results obtained in natural 
sleep and in that produced by such narcotics as veronal, trional, 
paraldehyde, and chloral hydrate. After the injection of scopola¬ 
mine, on the other hand, Kutner found that the tendon-jerks were 
never diminished, but usually active, and sometimes exaggerated, 
the ankle-jerks more so than the knee-jerks. In eight cases well- 
marked ankle-clonus was present. In one case a violent patient 
with absent tendon-jerks was given a subcutaneous injection of 
| milligramme of scopolamine. Ten minutes later the excitement 
was less, the tendon-jerks were active, and the plantar reflex, 
hitherto flexor, was now extensor. In sixty-three cases the plantar 
reflex was examined. In thirty-four cases sleep was spontaneous, 
in twenty-nine it was produced by veronal, trional, or chloral 
hydrate. In thirty-two patients, most of whom belonged to the 
dementia prsecox group, the response was always flexor. Of seven 
patients suffering from general paralysis, four showed slow dorsal 
flexion of the great toes, two in natural sleep, and two after trional 
and chloral hydrate respectively. All when awake had active 
tendon-jerks. In the other three Babinski’s sign was negative. 
The tendon-jerks in the waking condition were active in two and 



absent in the third. Of the remaining twenty-four patients who 
suffered from delirium tremens, seventeen showed a positive, seven 
a negative Babinski’s sign. Of the former, three were in a spon¬ 
taneous sleep; in the remainder, sleep was produced by paralde¬ 
hyde, veronal, or chloral hydrate. All when awake had active 
reflexes. J. D. Rolleston. 


(121) plantaire et le phdnom&ne des orteils (signe de Babinski) du 
point de vue physiologique et physio-pathologiqne.) Noica 
and Sakelaru, Semaine Midicale, Dec. 19, 1906. 

These writers examined carefully the exact nature of the plantar 
reflex in a large number of cases, both normal and abnormal. In 
normal cases they find there are two distinct plantar reflexes, the 
internal plantar reflex and the external plantar reflex, associated 
respectively with the first sacral and with the last lumbar roots. 
The internal plantar reflex, obtained by gently stroking the inner 
side of the sole, consists of flexion and separation of the last four 
toes, with, if more pronounced, flexion of the great toe; and, if 
still more marked, bending and rotation of the foot inwards. The 
external plantar reflex, obtained by stroking the outer edge of the 
foot, consists of flexion and abduction of the little toe; and, if 
more pronounced, of flexion of the last two or three toes at their 
metatarso-phalangeal joint with extension at the other joints. 

In a large number of patients, with various diseases of the 
nervous system, they found that the external plantar reflex was 
more readily elicited, and could be divided into eight different 
stages or degrees. Of these, the abduction of the smaller toes and 
the extension of the great toe, described by Babinski as indicative 
of an affection in the pyramidal tract, form two stages. 

The external reflex is almost, without exception, more readily 
elicited by stroking the outer side of the foot, and frequently the 
writers found the Babinski sign by stroking the outer side, while 
the ordinary flexor plantar reflex was got by stroking the 
inner side of the sole. 

The writers discuss the nervous and muscular mechanism by 
which the reflexes are produced, and give several references to the 
literature. John D. Comrie. 

BABINSKTS SIGN IN CHOREA (Signe de Babinski dans la chorde 

(122) de Sydenham.) A Charpentier (Soc. de NeuroL), Rev. Neurol., 
Dec. 30, 1906, p. 1176. 

A boy, aged twelve, had an attack of chorea following acute 
rheumatism. The irregular movements were generalised, but pre- 



dominated on the right side. The tendon-jerks were equal on the 
two sides, but there was a definite extensor response of the toes of 
the left foot, while on the right side the plantar response was 
normal. This fact, which should be compared with the combined 
flexion of the trunk and thighs found by Babinski in certain cases 
of chorea, seems to indicate that a perturbation of the pyramidal 
tract exists in that disease. J. D. Rolleston. 

Makuen, New York Med. Jowm ., Dec. 29, 1906, p. 1261. 

This is a paper read before the Eastern Section of the American 
Laryngological, etc., Society. The author, after emphasising the 
neglect of defects of speech alike by qualified teachers and practi¬ 
tioners (with the natural result that such patients too often pass 
into the hands of quacks), holds that the study of these defects 
belongs more to the laryngologist than the neurologist. After 
alluding to the unfortunate confusion of nomenclature in connec¬ 
tion with the subject, he adopts as the definition of stammering, 
“ a more or less constant inability to speak freely owing to an 
inco-ordinate and spasmodic action of the respiratory, phon&tory, 
or articulatory muscles.” 

He points out its prevalence amongst all nations, especially in 
childhood, and is evidently strongly impressed with the severity 
of the handicap placed by the condition on the patients, many of 
whom he even says “ die early, because having a weak nervous 
organisation to begin with they are unable to endure the strain 
placed upon them.” 

He then discusses the importance of constructing an alphabet 
of sounds, and “ receiving the suggestion from Melville Bell, 
Wyllie, and others,” gives the table of sounds which he has drawn 
up, and calls (after Wyllie) The Physiological Alphabet. The table 
given in the article is practically identical with Wyllie’s in every 
respect, even to the illustrative sentences ; but although he holds 
that the use of his alphabet teaches the stammerer “ the art of 
orderly thinking as well as orderly speaking,” and puts great 
stress on the need for pursuing the “ syllabication ” method in the 
treatment of pupils, he makes no reference to the important 
physiological difference (as regards their proper method of enun¬ 
ciation by the stammerer) between the consonants classed as 
voiceless and voiced respectively. Evidently the main point in 
his view is the cultivation of syllabic enunciation, each syllable 
“ requiring a separate and distinct respiratory impulse,” which the 
patient is taught to give. Hamilton G. Langwill. 



THUS TACTILE APHASIA. (La vraie aphasia tactile.) Ernest 
(124) Jones, Rev. Neurol ., Jan. 15, 1907, p. 3. 

A case of cerebral monoplegia was shown recently at the Neuro¬ 
logical Society of Paris, where the patient was unable to recognise 
objects placed in the paretic hand, and Raymond, considering the 
defect as of central origin, called it “ tactile aphasia.” Ddjdrine, 
however, maintained that the peripheral disturbances were 
sufficient to make recognition of objects impossible. Clapar&de 
returned to the subject at a later date, and showed the condition 
to be really one of “ tactile asymboly,” arguing that we cannot 
speak of tactile aphasia unless the patient knows what the object 
is, and how to use it, but fails to name it from touch. Such a 
tactile aphasia must obviously be very improbable, since our 
memory of words is associated more intimately with auditory and 
visual images than with the sense of touch. 

The author reports a case which he considers to be the first 
true case of tactile aphasia ever recorded. The patient was a man 
with hysterical right hemiplegia of traumatic origin, and of seven 
years’ duration. He presented characteristic symptoms of anal¬ 
gesia, allocheiria, etc. During treatment he began to improve 
steadily, and in an interesting way. At first he had complete 
anaesthesia, although when his attention was diverted it was easy 
to demonstrate that he did respond to external stimuli. This 
was the phase of psychical anaesthesia. Later, he was able to feel 
objects, while he could not recognise their form or localisation. 
This corresponded to the “ Tastlahmung ” of Wernicke. Later, he 
recognised the form of objects, but had a certain amount of 
persisting faulty localisation, and slight objective parsesthesia. 
If a coin were put into his hand, he said it was a piece of metal, 
round and flat, but did not know what it was. This should be 
described as tactile asymboly, for there was clearly no astereog- 
nosis. Finally, the asymboly vanished, and the patient was able 
to recognise objects placed in his hand, and to use them accurately, 
but he could not thus name them. For an instance, a friend gave 
him a screw-driver of a rather peculiar shape, and while he 
employed it properly, he could not give it a name, although he 
was familiar with tools. The moment he heard the name men¬ 
tioned, he knew it at once. The recognition of an object by touch 
depends first on the elementary sensations of touch, temperature, 
etc., then on the complex synthesis of these, and the resulting 
appreciation of form, surface, consistence, etc., then on the recogni¬ 
tion of the essential nature of the object, and finally on the 
recollection of its name. Stereognosis and the sense of localisation 
are complex, and depend on a psychological synthesis, which 
naturally must be central. A peripheral lesion may abolish all 



varieties of perception and recognition: if we cannot feel an object, 
we cannot recognise it. But it is possible to have a central lesion 
interfering with the identification of an object, though elementary 
sensations are not deranged. 

Tactile aphasia seems to correspond to the optic aphasia of 
Freund, and it should be distinguished from tactile asymboly in 
the same way as visual asymboly (“ Seelenblindheit ”) is to be 
distinguished from visual aphasia. S. A. K. Wilson. 


CONFABULATION. (Bur la confabulation et ses rapports avec la 
(125) localisation spatialo des souvenirs.) A. Pick, Archiv. de 
Psychol., Aug. 1906, p. 141. 

The term “ confabulation ” is a neologism fathered by certain Ger¬ 
man psychiatrists to denote the attempts of patients suffering from 
amnesia to supplement the gaps in their memory by recollections 
which are purely fanciful. It originates in the unconscious neces¬ 
sity the patient experiences of projecting into the past an ordered 
register of collateral events in which he can localise the ideas 
evoked by the examining physician or by himself. The need on 
which confabulation is based is closely akin to the common feeling 
of discomfort accompanying failure to get definite hold of some 
elusive recollection. In the diseased person the easy and speedy 
resort to confabulation prevents discomfort from appearing or 
becoming intense, while the normal person has to possess his dis¬ 
turbed soul in patience till the lacuna is bridged, because he can 
do nothing to meet the emergency. Another explanation of the 
need for confabulation is set forth in Stout's “Groundwork of 
Psychology.” This author refers the phenomenon to association, 
and shows that the events of a day, for example, however various 
in kind, leave in the memory a collective trace which can be re¬ 
produced en bloc. With this impression as a starting-point, com¬ 
ponent details can be made to surge up one by one in the memoiy. 
To localise a certain event in the past, as James points out, is to 
think of it in its immediate context. This remembrance by con¬ 
nection derives from the fact that every one of our actions, not 
only objectively but also psychologically, is for our ego but the 
fragment of a complicated whole. In states of weakened percep¬ 
tivity the recognition of persons or objects is further enfeebled 
when they are placed in an unusual milieu. The everyday en¬ 
vironment favours the linking up of associations. This localisation 
in space as opposed to that in time plays an important r61e in the 
functioning of the memory. How often are ungifted people un- 



able to speak of a fact without recounting ab ovo the whole series 
of events of which it is a part 

The author analyses a case where a healthy workman of 58 
was severely wounded in the right frontal region by a block of 
wood. Some bony splinters were removed, and a hernia cerebri 
treated. The patient remembered all about the accident, but was 
completely out of his reckoning in regard to space and time. As 
bis condition improved, he occupied himself regularly with house* 
hold tasks. The mechanical activities to which the patient had 
given himself over being deeply impressed on his nervous centres, 
were unaccompanied by confabulation, whereas a whole aureole of 
imaginary memories burst forth to furnish a setting of time and 

Heilbronner explains the rarity of confabulation in eclomptics 
by the marked dissociation of ideas which prevents gaps in the 
memory being felt at all. 

The relations between amnesia and confabulation fall into three 
groups: (1) simple defect of memory, (2) defect of memory with a 
struggle against confabulation, (3) defect of memory with confabu¬ 
lation more or less marked. These varieties cannot be supposed 
to be the consequence of arrested development, as in the case of 
the untruthfulness of abnormal children, and are more likely to 
correspond to a dissolution. J. Rot Tannahill. 

(126) of Abnorm. Psych., December 1906. 

The patient was a healthy, robust, middle-aged woman, of a very 
religious mind, and the wife of a clergyman. In early childhood, 
at the request of her father, she performed automatic writing on 
the planchette. Many years later experiments were carried on 
with the planchette, under the direction of her husband; she was 
unconscious of what was done by the planchette until it was told 
to her. 

The subconscious writing showed supposed communications 
from deceased persons; accounts of life on the planet Mars, of 
which maps were drawn, zones indicated, inhabitants described, 
and evidence of the Martian language manifested. The author 
first saw the case in 1900 ; the Martian episode was resumed and 
a language was somewhat imperfectly developed. It is to be 
noted that in 1900 a somewhat unusual interest had been 
aroused by current literature in the planet Mars, which the patient 
uiay have read. Nevertheless more must be known about sub¬ 
liminal creations before one could establish an intelligible relation¬ 
ship between such coincidences. 

Another personality called Harrison Clarke presented itself; 



normal mirror and inverted writing could be used by the new per¬ 
sonality. This personality, in response to the demand for proof of 
his identity, told a story, the falsity of which could be demon¬ 
strated ; when the character was confronted with the facts he 
admitted their embarrassing character, but insisted upon “his 
reality as a discarnate spirit” 

In looking for an explanation of these phenomena, if one turns 
to the subconscious mental action of the individual he will find a 
general source which cannot be doubted. To give a definite reason 
for the peculiarities of the phenomena in any given case such as 
this would be difficult. The process itself is one of “ interrupted 
association in subconscious activity and its casual influence on the 
motor system.” The nearest description to what occurs may 
perhaps be stated as “ a partial suspense of muscular tonicity to 
allow the subliminal action to let occasional subconscious ideas 
slip through.” C. H. Holmes. 

(127) nach Augenoperationen.) M. Lapinsky (of Kiev), Allg. Ztsehr. 
f. Psych. , Bd. 63, H. 5. 

The patient was a poorly-nourished man, 60 years of age, with 
marked arterio-sclerosis, gastric disorder, and ulceration of the 
cornea, secondary to trachomatous contraction of the eyelid. 
During treatment for his eye trouble, which necessitated rest in a 
fairly dark room, he developed acutely a typical hallucinatory 
confusion such as one meets in arterio-sclerotics. One could ex¬ 
clude drugs as an axiological factor. After discussing the case 
and reviewing the literature, the following conclusions are given: 
In psychoses following an operation on the eye there is, as a rule, 
no setiological connection between the two. Psychoses after eye 
operations usually occur in advanced life; such psychoses have no 
specific features. The author considers that in these arterio¬ 
sclerotic cases the patients are especially susceptible to toxic 
influences; in the case recorded the toxic influence had its source 
in the disordered alimentary system of the patient. 

C. Macfie Campbell. 

(128) (Beitrag znr Klinik der Puerperalpsychosen, Generation- 
psychosen.) G. Herzer (of Basle), Allg. Ztsehr. f. Psych., 
Bd. lxiii., H. 2. 

An analysis of the cases admitted to the Basle Clinic during the 
last twenty-five years, based on the classification of Kraepelin, with 



special reference to the frequency and form of puerperal psychosis, 
their relation to the different periods of child-bearing, their course 
and prognosis and relation to heredity, number of births, and other 
etiological factors, such as infection, trauma, etc. The material 
embraces 221 cases, forming ll'7/£ of the female admissions. The 
detailed results cannot be summarised. C. Macfie Campbell. 

(129) (Znr Aetiologie und Symptomatology dor Katatonie.) Pfistkr 
(of Freiburg), Allg. Ztschr.f. Psych., Bd. Ixiii., H. 2. 

Patient was a young man of normal development until 1881, 
when, at the age of 15, he received a severe blow over the left 
parietal region, some fragments of bone having to be removed by 
operation. Patient appeared to recover completely; later a slight 
change in character was noticed—obstinacy, irritability, and later 
increasing intolerance of alcohol. There was also headache of 
variable intensity and tremor of the hands. In 1890 he was brought 
to the psychiatric clinic owing to the development of paranoic 
ideas, which consisted chiefly in ideas of persecution by his family; 
he was soon discharged, but in 1894 he was readmitted on similar 
grounds, with ideas of reference and auditory hallucinations; after 
five months he was again discharged improved, but was read¬ 
mitted in 1897; he was suspicious and did not answer frankly, 
showed marked negativism, was evidently annoyed by constant 
auditory hallucinations. During the further course of his dis¬ 
order, patient showed a well-marked catatonic picture with 
impulsive acts, stereotyped movements, mannerisms of speech, 
unmotived repetitions of the same phrases, negativism, mutism, and 
peculiarities of writing. He distorted the words by inserting after 
almost every vowel s or h or t, frequently doubled the diphthongs 
and the final consonants. His speech was defective, showing at 
an early date stammering and a difficulty resembling that of the 
general paralytic; the intonation was very monotonous, and he 
frequently repeated phrases. The dysarthria became more marked 
during the further course of the disease. The author considers 
that the trauma had given rise to a traumatic neurosis, which might 
be called neurasthenia, and that later on the basis of this, a slowly 
developing catatonic deterioration-process, had followed. Even 
when the whole disease was well established, the neurasthenic 
complex existed side by side with the other symptoms. There was 
tremor of hands and tongue, vasomotor excitability, increase of 
the reflexes, headache, and intolerance of alcohol. He considers 
that the trauma might be of setiological importance in two ways, 
and takes for granted that auto-intoxication is at the basis of the 



catatonic process. The trauma, therefore, might have caused 
either a general inability of the brain tissue to satisfactorily dis¬ 
pose of its waste products, or it might have caused an auto-intoxi¬ 
cation by directly implicating hypothetical regulating centres of 
metabolism. He considers that as a rule the aetiological import¬ 
ance of trauma is exaggerated. In traumatic hysteria, neurasthenia, 
and the functional psychoses, trauma is merely a precipitating cause, 
the psychosis being equally due to the special constitution which 
gives the definite reaction. 

With regard to the details of the case, he discusses especially 
the speech and writing defects. The writing defect had shown 
itself at an early date, and had at first been looked upon as a focal 
symptom; the further course of the disease made this view un¬ 
tenable, but the author considers that the local injury was perhaps 
a predisposing cause for the catatonic symptoms showing a certain 
elective severity in the speech realm. In addition to his intoxica¬ 
tion hypothesis, he calls in the individual disposition as a possible 
explanation of the fact that in different catatonics different groups 
of symptoms are prominent. In some cases the greatest disorder 
is seen in the movements of expression, in others in their speech, 
in others in gestures and general behaviour. He has observed 
that those catatonics who show most marked speech disorder are 
those who are constitutionally “ motor ” in the sense of the French 
authors. C. Macfie Campbell. 

(130) (of Philadelphia), Joum. Am. Med. Ass., January 5, 1907. 

The author asks two questions: (1) Is trauma in itself a true 
cause of insanity ? He believes that trauma must have a suitable 
soil, such as unhealthy ancestry, cerebral arterial disease, syphilis, 
alcoholism, etc., otherwise insanity will not develop. (2) (a) Does 
any characteristic type of insanity follow trauma ? ( b ) From the 
mental symptoms alone can it be told that a man is insane on 
account of having received a trauma ? He believes that there is no 
characteristic type of post-traumatic insanity; the most common 
symptoms of this condition are confusion, delusions, simple 
dementia, and epileptic insanity. He has never seen “ true melan¬ 
cholia” or paranoia follow an injury. He gives the case histories 
of seventeen patients, in whom the relation between the injury and 
the development of insanity was sufficiently close to make it 
reasonable to believe that the development of insanity was not a 
mere coincidence. Among these cases there were five in whom 
excessive alcoholism was thought to have played an important 
part; six were of advanced age; three suffered from general 



paralysis; one showed distinct involvement of the left temporo- 
aphenoidal lobe and reacted to auditory hallucinations; one was 
constitutionally inferior; one became confused after an injury to 
the back. The author repeats that in none of these cases could 
traumatism alone be considered as the cause of insanity. 

C. H. Holmes. 


(131) TUMOURS OF THE CEREBRUM. Charles H. Frazier, 
Med. Bull. Univ. of Penn., April-May 1906. 

Many different opinions have been expressed as to the operability 
of cerebral tumours owing to the various interpretations which 
have been applied to the word operable. Walton and Paul, from 
statistics of the clinical and post-mortem records of 424 cases of 
cerebral tumour, classed 7 per cent, as operable, 80 per cent, as 
inoperable, and 13 per cent, as doubtful. Prof. Frazier points out 
that they used the term operable as practically synonymous with 
curable, and further, that their statistics were based upon cases in 
which the tumours had reached such a size as to cause death. It 
is obvious that from a study of such cases the number of operable 
cases is at a minimum. Prof. Frazier passes at once to the practical 
side of the question—the advisability of operation in cases of 
cerebral tumour. His opinion is that operation should be under¬ 
taken in every case in which relief from suffering can be secured 
for any considerable period. It is important to note that by 
operation he does not necessarily imply an attempt at the removal 
of the growth. In a few favourable cases operation may result in 
the complete removal of the tumour and the cure of the patient. 
In other cases the tumour may be removed in whole or in part 
without much prospect of cure, but with great temporary benefit 
to the patient. In other cases it may be possible to relieve the 
patient’s suffering and to preserve his sight although it is im¬ 
possible to remove the growth. Before advising an operation the 
first point to be determined is the situation of the growth and 
whether it is accessible to the surgeon, the most favourable 
situation being the surface of the brain on its extreme aspect. If 
the tumour be accessible, an operation should be performed to 
expose it If the tumour be exposed, then the question as to its 
removal has to be decided. This depends on the size and nature 
of the growth. If the growth is infiltrating and of wide extent, 
the author holds strongly that its removal should not be attempted 
—(1) because such growths are very vascular and the risk of an 
immediate fatal issue from haemorrhage is very great; and 



(2) because such growths can never be removed in toto and are 
liable to recur, and grow more rapidly after they have been inter¬ 
fered with. These are the general lines which Prof. Frazier lays 

In cases where the tumour has been localised, but is not exposed 
at the time of operation, he advises that small exploratory incisions 
should be made into the brain, as otherwise a tumour might quite 
well escape detection. 

The technique of the operations and the various openings which 
he makes for exposing the different regions of the brain are fully 
described, and mention may be made of one or two of the points 
on which he lays stress. (1) The mapping out of the flap before 
the operation. (2) Osteoplastic operation. (3) The administration 
of ether as an anaesthetic instead of chloroform. (4) The frequent 
observation of the blood pressure as an accurate guide to the 
condition of the patient. (5) The performance of the operation in 
one stage. T. Grainger Stewart. 


B. Sachs, Medical Record , Dec. 22, 1906. 

This article is devoted to the consideration of the surgical treat¬ 
ment of tumours of the cerebellum, or rather of cerebellar tumours, 
under which name the author apparently includes tumours situated 
outside the cerebellum. 

The author desires to see the results of all operations on 
tumours of this region published, the failures as well as the 
successes, as he holds that an erroneous idea as to the success of 
operative interference has been created by the publication of 
successful cases only. During the past few years he has observed 
22 cases of cerebellar tumour; of these, 7 were operated upon. 
In 4 cases attempts at removal of the tumours were undertaken, 
with fatal results; but in 2 of these cases, in which the side of the 
growth had been correctly diagnosed, the growths were not found 
at the time of operation. In 3 cases palliative operations were 
undertaken with benefit to the patients, pressure being relieved 
and vision preserved. In the other cases no operation was under¬ 
taken. These results have led the author to conclude that the 
present state of cerebellar surgery is not such as to warrant 
attempts being made at the removal of cerebellar tumours, and 
that palliative operation for the relief of pressure and of the neuritis 
is all that can be justifiably advised. The author admits that none 
of the cases were cured, and that those which were not operated 
on became blind; but holds that early palliative operation, although 



not curing the patient, prolongs his life, preserves his sight, and 
rids him of his headache. There is, however, no attempt made 
to distinguish between the results of operation on cerebellar 
tumours proper, and tumours situated in the angle between the 
cerebellum and the pons, and indeed the author seems to class 
them together. The dangers and difficulties attending an opera¬ 
tion for the removal of a tumour from the lateral lobe of the 
cerebellum are not to be compared with those incurred in an 
attempt to remove an extra-cerebellar tumour. 

T. Grainger Stewart. 

(133) diagnostische Himpunktion.) M. Ascou, Berlin, klin. 

JFchnschr., Dec. 17, 1906. 

The following method of performing this operation was devised by 
A Kocher in 1899: After preparation of the parts in the usual 
way, a drill is inserted through the soft tissues, the bone perforated, 
and a Pravatz syringe introduced through the perforation. This 
form of exploratory puncture was employed by Th. Kocher in his 
Clinic, both as a therapeutic measure for the injection of tetanus 
antitoxin into the brain and evacuation of fluid from the ventricles, 
and as a means of diagnosis. The technique of the operation, as 
performed by Neisser and Pollack, is as follows: With a fine 
gimlet they pierce the soft tissues and bone, using instead of the 
drill an electric dental engine, and they have found the procedure 
of material service both from a diagnostic and therapeutic point of 
view. In spite of this, however, Ascoli says this important opera¬ 
tion has not been extensively employed. With regard to the 
Neisser-Pollack method, he considers the current from the electric 
dental engine difficult to control, and has substituted in his cases 
an ordinary dental engine, to which the fine drill is attached. The 
foot motor is unsuitable with cocaine anaesthesia, as the operation 
is not so quickly accomplished. In using the ordinary dental 
engine the handle must be held in the same way as a pen, the 
elbow being firmly supported, so as to avoid injury to the dura or 
brain, and the ball of the little finger resting on the head of the 
patient. The drill should perforate the bone in a perpendicular 
direction. It is set in full motion, and lightly pressed on the 
selected spot Sudden cessation of resistance indicates completion 
of the perforation, and the drill should be immediately stopped by 
pressure upon the knob of the handle, which is now removed, the 
drill being left in situ. Slight displacement of the soft tissues on 
removal of the drill sometimes renders it difficult to find the 
perforation and insert the exploratory needle, and Ascoli has 



endeavoured to obtain fixation of the skin by means of a groove 
in the drill 8 mm. in depth, which on the completion of perforation 
sinks down and presses on the skin, but the results have not been 
altogether satisfactory. The method he now employs is to bind 
two parallel bands round the head of the patient at a distance 
of 1 centimetre, the spot chosen for puncture lying between them, 
and this, combined with fixation of the skin by the finger, appears 
to him to facilitate the finding of the perforation. In selecting 
the point of puncture, risk of injury to the vessels should be 
avoided (the art. meningea media and the venous sinuses), and 
one should be guided by the symptomatology and the anatomical 
characteristics. Neisser and Pollack employ Kocher’s cyrtometer 
as a means of cranio-cerebral topography. As regards the depth 
to which the exploratory needle should penetrate, one must be 
guided by the symptoms in individual cases and the condition of 
the affected parts. When the focus of disease is deeply situated, 
radical surgical operation is rendered impossible, so that the 
advantage of deep puncture is more apparent than real, and it 
also involves the risk of injury to the vessels. Details of six 
cases treated by this method are given at the conclusion of the 
article. In one of these a diagnosis of cystic tumour of the right 
hemisphere of the cerebellum was made from microscopic examina¬ 
tion of particles of the tumour removed by aspiration and the 
chemical characters of the fluid, and section showed a glio-sarcoma 
of the right hemisphere of the cerebellum. In another case 
puncture indicated disease of the left cerebellar hemisphere, and 
the case was diagnosed by exclusion as a tuberculous tumour, the 
sterility of cultures on the ordinary media negativing the presence 
of quickly growing abscess. In a further case the results of 
puncture were negative, while section revealed a tumour of the 
base of the brain, showing that a diagnosis based on negative 
results of puncture is not infallible. In another case the diagnosis 
of haemorrhage of the arteria meningea media was confirmed on 
section. In one case penetration was accomplished in an unusually 
short time, the syringe being filled with cerebro-spinal fluid at 
a depth of 3 centimetres, and at the autopsy hydrocephalus was 
found, secondary to tumour at the base of the brain. Up to the 
present time, though the results of the procedure have not been 
wholly satisfactory, no unfortunate complications or results have 
occurred in the cases operated upon by the writer. He is of 
opinion that the operation should not be indiscriminately under¬ 
taken, but employed with care. On the other hand, he hopes that 
further experience will definitely establish the safety of the 
procedure, as in certain cases it is the one and only means of 
averting a fatal termination. Donald Abmoub. 




EINIOEB 8AUOETIEEE. J. P. Karplus. Pp. 162. Wien: 
F. Deuticke. (Otto Schulze & Co., Edinburgh.) 1907. 10 M. 

The anatomy of no other organ of the body has been so minutely 
studied as that of the brain, and owing to this fact, as well as to 
the complexity of its structure, there is no organ more suitable 
for the investigation of the hereditary transmission and the varia¬ 
tion of characters. Karplus has already published an interesting 
monograph on the similarity of the fissuration of the fore-brain 
in different members of the same family, in which he showed 
that, in man at least, peculiarities in the brain sulci may be 

In the book under review the conclusions he then obtained 
are shortly summarised, and the results of the minute investigation 
on the variation in hereditary characteristics as revealed by the 
study of a much larger material is published for the first time. 
In twenty cases he was able to examine the brains of two members 
of the same family, in five cases the brains of three members, and 
finally in one case the brains of five members of a family. In 
addition to this he studied the nervous systems of four members 
of the families of an ape, of a bitch, and of a cat, and the brain of 
a goat and its twin kids. 

His observations are in every case given in tables so arranged 
that the peculiarities common to, or the variations found in, the 
different members of a family can be easily compared. The con¬ 
clusions of his previous work on the human brain are confirmed, 
viz. that there is a general similarity between the brains of 
different members of a family; but in the macaque monkey 
similarity is rarely observed between the furrow arrangement in 
the brains of a mother and of her offspring. In the monkey the 
two hemispheres of a brain are generally very much alike, while 
in the human brain there is almost invariably marked dissimilarity 
between the two hemispheres. This suggests that in the course of 
phylogenetic development the original symmetry in the fissuration 
of the two sides of the brain is gradually lost, and that the sulci of 
each hemisphere attain a greater permanency and become less liable 
to variation. 

The book is an interesting contribution to the study of heredity 
and opens up a new and promising field for exploration. It is well 
illustrated. Gordon Holmes. 




Paris: Masson & Son. (Otto Schulze & Co., Edinburgh.) 

1906. 8fr. 

Dr Zimmkrn’s book on Medical Electricity is well arranged, and 
contains a considerable amount of matter which one does not meet 
with in similar English treatises. Little attention is given to 
details of apparatus, but this enables more space to be allocated to 
discussing those physiological actions of electricity on which the 
methods of electrical treatment are necessarily founded, a long 
chapter being devoted to the excito-motor action of electricity, 
and a shorter one to the sedative applications of an electrical 
nature. Recent work is introduced on the theory of Ions and 
the introduction of medicines by electrolytic methods. Another 
chapter discusses modern researches on the resistance of the living 
body; whilst the final chapter, whose chief fault is that in some 
respects it is too brief, deals with the uses of electricity in various 
pathological conditions. 

The book is interesting and valuable as reflecting the present 
state of electro-therapeutics in France, where, in many respects, it 
is better understood and more highly valued than it is in this 
country. Harry Rainy. 


Wilhelm Furnrohr. Berlin: S. Karger. 1906. M. 10. 

Dr Furnrohr’s book deals with a limited section of research in 
the department of X-ray work, but within this it is fairly 
complete. Like most German treatises it contains a lengthy 
literature index, compiled rather with a view to volume than 
value, in which the productions of the Fatherland occupy a 
predominant position. 

The text discusses Diseases of the Brain and Skull, of the 
Spinal Cord, Vertebrae, and Peripheral Nerves, as well as the 
various Neuroses, and probably contains all that is of importance 
to know in these subjects in relation to X-ray work. The book 
is largely illustrated by actual X-ray photographs taken in the 
various conditions. The illustrations are of only moderate clear¬ 
ness, and do not in themselves give one any great impression of 
the value of radiography; but this is partly due to the inadequate 
methods adopted for their reproduction. 

The general impression which one receives from a perusal of 
the book is that the contributions which are likely to be made 
by radiography to pure neurology are not of very great importance, 
although, in the case of tumours arising from neighbouring bony 
structures, this method may enable a diagnosis to be more 
certainly arrived at Harry Rainy. 





REMY COLLIN. Recherches cytologiquee sur le d6veloppement da la cellule 
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GO WEN. Some Aspects of Pestilences and other Epidemics. Am. Journ. of 
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MARINESCO. La nature intime du prooeesus de d£g£n6rescence dee nerfs. 
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LEVI. Studien zur normalen und pathologisohen Anatomic der hinteren Riicken* 
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ORZECHOWSKI. Riicken marksbef unde bei Amputationsf&llen der oberen 

Extremitat. Arbeit, a. d. neural. Instil, a. d. Wien. Univ., Bd. 13, 1906, S. 97. 
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MARBURG. Hypertrophie, Hyperplasia und PseudohypertropMe des Gehirns. 
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W. MAULE SMITH. An Investigation into the Arrangement of the Achrom&tio 
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ian. 30, 1907, p. 90. 

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OTTO RANKE. t)ber Gewebsver&nderungen im Gehim leutischer Neugeborener. 
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OTTO RANKE. Uber Gewebsveranderungen im Gehirn leutischer Neugeborener. 
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VERSB. Periarteritis nodosa und Asteritis syphilitica oerebralis. BeiL our 
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Anat. und allg. Path., Bd. 40, H. 3, 1907, p. 601. 



PAGE. Les Troubles digestifs consid£r6s dans leurs rapports avec les troubles 
nerveux et mentaux. G&inch, Paris, 1907. 


LIEBERS. Ein Fall von Dystrophia musculorum progressiva kombiniert mit 
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CHARLES E. INGBERT. Pseudo-Hypertrophic Muscular Atrophy. Journ. 

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RAYMOND. Sur quolques affections des nerfs plripheriques. Oaz. de* h6p., pp. 
135 and 147. 

DEJtiRINE et THOMAS. Sur la nlvrite interstitielle hypertrophique. Now. 
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JAMES SHERREN. A Clinical Lecture on a Case of Secondary Suture of the 
Great Sciatic Nerve. Bril. Med. Joum. % Feb. 16, 1907, p. 867. 

DERCUM. Diagnosis and Treatment of Multiple Neuritis. Therapeutic Gazette, 
Jan. 15, 1907, p. 10. 

FRANCEZ. Beri-beri, its history, symptoms, causation, and treatment. N. Y . 
Med. Joum., Feb. 9, 1907, p. 263. 

iran CORE— 

Taken. —ZACHARTAS. Kine Geburt bei vorgeechrittener Tabes dorsalis. Miinch. 
med. WocL y Feb. 12, p. 321. 

MAURICE FAURE. The Treatment of Tabetic Ataxia by Methodical Exercises. 
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GIDON. Amelioration symptomatique d’un pas de tabes par les applications 
locales de H. F. Bull. de la Soc. Franfais & RlectroOUr. , f&v. 1907, p. 41. 

FrleRreich's Ataxia. —DEJERJNE et ANDRlfc THOMAS. Les lesions des raoines, 
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poliomyolit. an. ac. i Hvaler l£ge-distrikt sommeren 1904. Norsk Magas, for 
L&gecid. , 1906, S. 409. 

■eredltary Paraplegia.— ERNEST JONES. Eight Cases of Hereditary Spastic 
Paraplegia. Rev. Neurol, and Psyckiat. 9 Feb. 190/, p. 98. 

Marmis ated Sclerosis* —O. M A AS. Beitrag zur Prognose der multiplen Sklerose, 
Berlin, klin. WocK., Feb. 18, p. 197. 

NAMBU. Zerebrospinale Herdsklerose mit selten hochgradige Affektion des 
Riickenmarks. Prog. med. Woch. , Jan. 17, p. 27. 

RETHI. Die laryngealen Erschcinungen bei multipler Sklerose des Gehirns und 
des Riickenmarks. Safar, Wien, 1907, M. 4. 

SyriBfomyflla.— FRIES. Die Syringomyelie in Senium. A rbeit . a. d. neurol. Instil, 
a. d. Wien. Univ.i Bd. 13, 1906, S. 170. 

LEJONNE et CHARTIER. Syringomyelie consecutive h I’lcrasement d’un 
doigt. (Soc. de Neurol.) Rev. Neurol ., jan. 30, 1907, p. 79. 

Tiissr.—E. W. TAYLOR. Tumour of the Spinal Cord leading to Destruction 
of the Lumbar Region, Hydrocephalus, Double Optic Neuritis, and Painless 
Labour. Boston Med. and Surg. Joum. , Feb. 7, 1907, p. 161. 

OOURBOULES. Contribution k 1’ltude des tumeursde la moelle. ( Thise.) Rey, 
Lyon, 1906, 2 fr. 

Spinal Carles. —ALQU1ER. Quinze autopsies de mal de Pott chez l’adulte. 
None. Icon, de la Salp$(riire t nov. -d6c. 1906, p. 510. 

ALQUIER. Les Accidents nerveux du mal de Pott chez les adultes. L'Enctphale , 
Annie 2, No. 1, 1907, p. 48. 

CALOT. Traitement Rationnel du Mal de Pott k l’usage des Praticiens. Octave 
Dom, Paris, 1906, 3 fr. 


Meningitis. —La mlningite ourlienne. Rev. nuns, des Maladies de C Enhance, flv. 
1907, p. 78. 

RE1MANN. Meningitis cerebrospinalis; Heilung. Prog, med . Woch. 9 Jan. 31, 
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8PERONI. Cellules de l'exsudat dans la mlningite clrlbro-spinale Ipidlmique. 
La Preset mfd ., flv. 6, p. 82. 

ALEXANDER BERG. Et Tilfttlde af blandings-infektion red epidemisk cerebro¬ 
spinal-meningit. TidsJtr. /. d. nortke L&peforening\ 1906, S. 221. 

Epidemic ana Sporadio Meningitis. Editorial. Bril. Med. Joum., Feb. 16, 1907, 
p. 887. 



J. SINGLETON DARLING and JAMES WILSON. A Cue of Cerebro-spinal 
Meningitis, with Observations on a Pleomorphic Diploooocus obtained by Lumbar 
Puncture. Brit. Med. Joum., Feb. 23, 1907, p 433. 

CLOT. Mlningite tuberculous© du nourrisson. (Thhe.) Rey, Lyon, 1906, 
fr. 1.50. 

Encephalitis. —ALQUIER et BAUDOUIN. M6ningo-enc6phalite subaiguti ches 
un tuberculeuz. ^4rcA. de mid. expir., jan. 1907, p. 18. 

LAIGNEL LA VASTINE et ROGER VOISIN. Anatomie patholog. et pathogdnie 
de l'Enclphalite aigue. Arch, de mid. expir., jan. 1907, p. 28. 

CHAS. K. MILLS. Circumscribed Haemorrhagic Cortical Encephalitis. Rev. 
Neurol. and Psychxat Feb. 1907, p. 89. 

Apaplexy.— HOCHHEIM. Ein Fall von traumatisohe Spatapoplexie. MUnch. 
med. I Voch., Jan. 29, p. 214. 

■enlplcfla.—BYCHOWSKI. Zur Phanomenologie der oerebralen Hemiplegie. 

Neurol. Central W., Feb. 15, 1907, S. 164. 

L. BARD. Des contractures post-hemipldgiques pseudo-pr£coces. La Sim Mid., 
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POIREL. De l'hgmiclonotonie post-h6mipl£gique. (Thhe.) Barbier, Nancy, 

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W. C. KRAUSS. Tumour of the right versus tumour of the left frontal lobe of 
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CHARLES BEEVOR. Lettsomian Lectures on the Diagnosis and Localisation of 
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CHARLES E. BEEVOR. Lettsomian Lectures on the Diagnosis and Localisation 
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Bereich des zentralen Nervensystems. Karger, Berlin, 1907, M. 8. 

SEIFFER. t)ber die Geschwulste des Kleinhinis und der hinteren Schadelgrube. 
Urban & Schwarzenberg, Berlin, 1907, M. 1. 

CHABARDES. Des tumeurs c£r6bnales k forme psychoparalytique. (Thhe.) 
Rey, Lyon, 1907, fr. 1.75. 

MATHIEU. Contribution k l*6tude des tuberculomes m^dullaires. {Tkhe.) 
Barbier, Nancy, 1906, 

Echinococcus* — L. JACOBSOHN. Ueber Cystioercus cellulosae oerebri et muscu¬ 
lorum. Monatsschr. /. Psychxat. u. Neurol ., Feb. 1907, p. 119. 

Abscess.—NEUMANN. Der otitische Kleinhiraabezess. Deuticke, Wien, 1906, 

M. 3.60. 

Cerebral Diplegia.— ALFRED GORDON. Cases allied to Amaurotic Family 
Idiocy. N.Y. Med . Journ., Feb. 16, 1907, p. 294. 

General Paralysis. —HERMANN. Ueber organische Kontrakturen bei progree- 
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A. MARIE. Quelques photographies d’Arabes svphilitioues et paralytiques 
g£n£raux. Nouv. Jeon, de la Salpitrihre , nov.-d6c. 1906, p. 592. 

POUL HEIBERG. Die Zahl der Syphilis-F&Ue in Kopenhagen und die Zahl der 
an progressiver Paralyse in Skt Hans Hospital Gestorbenen. Centralbl. /. Ner¬ 
venheilk. u. Psychiat ., Feb. 15, 1907, S. 126. 

Trauma.—HARVEY CUSHING. On some Remote Consequences of Cranial 
Injuries. N. Y. Med. Journ., 1907, pp. 97, 161, 208. 


SCHNYDER. Alcool et Alpinisme. Anh. de Psychol., T. vi., No. 23, 1907, 
p. 209. 


BIANCHI. A Text-Book of Psychiatry for Physicians and Students. Translated 
by J. H. MacDonald. Baillfere, Tindall k Cox, London, 1906, 21s. 

J. S. BOLTON. Amentia and Dementia. Joum. of Ment. Set., Jan. 1907, 
p. r ,84. 



J. F. TOCHER. Hie Anthropometric Characteristics of the Inmates of Asylums 
in Scotland. Biometrika, Feb. 1907,- p. 298. 

GAUPP. Wege und Ziele psychiatnscher Forschung. Laupp, Tubingen, 1907, 

MERC IE R. Etude sur les variations de la pression arterielle dans les maladies 
nerveuaes et p&rticulierement les psychoses. ( Thlse.) Rey, Lyon, 1906, 2 fr. 
GALTIER. Contribution k l’urologie clinique des Psychoses d’origine exo- 
toxique, en p&rticulier de la psychose alcoolique. Vigot frferes, Paris, 1907, 2 fr. 
PITOIS. Etude generate de l’etat peychique ches les cardiaques. (Thlse.) Rey, 
I yon, 1906, fr. 2.25. 

C. W. BURR. Trauma of the Head as a Cause of Insanity. The Joum. of Am. 
Med. Assoc., Jan. 5, p. 33. 

M A RAN DON de MONTYEL. l/imitation psyohique, normale et morbide. 
(Suite.) Joum. de Neurol ., jan. 20, 1907, p. 30. 

BERTIN1. La rappresentaaaone e la valutazione dello spaiio lineare in rapporto 
col senso dello sforso nei sani e negli alienati. Ann. di Freniatria , Vol. xvi , 
f. 4, p. 323. 

C. G. JUNG. Cber die Psychologic der Dementia praecox. Marhold. Halle, 
1907, M. 2.50. 

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mid., jan. 1907, p. 116. 

MASSELON. La Melancholia ; Etude Medicale et Psychologique. Felix Alcan, 
Paris, 1906, 4 fr. 

A. GREGOR. Be it rage zur Kenntnis der Gedkchtnissttirung bei der Korsakoff* - 
schen Psy chose. Monatsschr. f. Psychiat. u. Neurol ., Feb. 19u7, p. 148. (Schluss.) 
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e fine.) Ann . di Freniatria , VoL xvi., f. 4, p. 305. 

Mental Prophylaxis in Childhood. Leading Article. Bril. Med. Joum., Feb. 16, 
1907, P. 399. 

W. MABON. The Open-air Treatment of Psychiatry. New York Med. Joum., 
Feb. 9, 1907, p. 241. 


Epilepsy.—PUCHENOT et CASTIN. Un cas d’etat de mal 6pileptique traite par 
laponction lombaire. Enciphale , Annie 2, No. 1, 1907, p. 71. 

ALQUIER et ANFIMOW. Existence et signification de petites Hfimorragies 
sous la Piemfcre cerebrals dans l’Epilepsie. (Hoc. de Neurol.) Rev. Neurol. , jan. 
30, 1907, P. 89. 

PAUL MASOIN. Application de la diazo-rlaction urinaire au pronostic de 
l'etat de mal 6pileptique. Joum. de Neurol ., jan. 20, 1907, p. 21. 

BERTINJ. La riprodusione grafioa ad ocohi chiusi di Curve circolari di deter- 
minato Diametro nei sani e negli epilettici. Ann. di Frtniatria. Vol. xvi, f. 4, 
p. 329. 

FREY und FUCHS. Reflexepilepsie bei Ohren- und Nasenkrankungen. Arbeit, 
a. d. neurol. Instil, a. d. Wien. Untv., Bd. 13, 1906, S. 78. 

SEGLAS. Crises de petit mal tpileptique avec aura jparamnlsique ; illusion de 
fausee reconnaissance. Rev. Neurol. , jan. 15, 1907. p. 1. 

MATHEW WOODS. The Relation of Alcoholism to Epilepsy. The Joum. of 
Am. Med. Assoc. , Feb. 9, 1907, P. 469. 

JOHN TURNER. Pathological Anatomy and Pathology of Epilepsy. Joum. of 
MenL Sci., Jan. 1907, p. 1. 

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p. 165. 


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FILIPPO LUSSANA. LTnfluenza del]' aloool aopra il rifleeso termocutaneo del 
tono *pin&le dei musooli volontari. Arckiv di Fisiologxa ? Nov. 1906, p. 74. 
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1906, 3 fr. 

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la cerveau. Montligeon , 1907. 

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muni ent*— 

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1907, p. 213. 

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Lancet , Feb. 2, 1907, P. 276. 

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Sickness. Lancet, Feb. 2, 1907, p. 282. 

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S. 128. 

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Nervenkrankheiten. Konegen, Leipzig, 1907. 

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und pbyriscbe Behandlung. Elischer Nachf., Leipzig, 1907, M. 1.50. 

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verwandten Erscheinungen. Fiedler, Leipzig, 1907, M. 3. 

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B&illifere et tils, Paris, 1906, fr. 1.50. 

* A number of references to papers on Treatment are included In the Bibliography under the 
fndfrldnal Diseases. 


L. Vernon Briggs. “ Observation Hospital for Mental Disease.” Boston 
Med. and Surg. Joum., 1906. 

L. Vernon Briggs. “ Observation Hospitals or Wards for Early Cases of 
Mental Disturbance.” Boston Med. and Surg. Joum., 1906. 

C. K. Mills. “ Unilateral Ascending Paralysis and Unilateral Descending 
Paralysis.” Joum. Amer. Med. Assoc., 1906. 

C. K. Mills and T. H. Weisenberg. “The Subdivision of the Representa¬ 
tion of Cutaneous and Muscular Sensibility and of Stereognosis in the Cerebral 
Cortex.” Joum. Nerv. and Ment. Dis., 1906. 

Crouzon. “ Titres et Travaux Scientifiques.” Steinheil, Paris, 1907. 

Morton Prince. “Hysteria from the Point of View of Dissociated 
Personality.” Heath & Co., Boston, 1906. 

C. G. Jung. “Uber die Psychologie der Dementia praecox.” Marhold, 
Halle, 1907. 

Bianchi. “Text-book of Psychiatry.” Translated by J. H. Macdonald. 
Baillifere, Tindall & Cox, London, 1906. 21s. 



“ Juristisch-psychiatrische Grenzfragen,” Bd. 6, H. 6. Vereinigung fur 
gerichtliche Psychologic und Psychiatrie im Grossherzogtum Hessen. Marhdd, 
Halle, 1907. M. 1.20. 

L’EnedphaU, No. 1, Ann4e 2, 1907. Delame, Paris. 

Neuropathological Papers, Harvard Univ. Med. School, 1905. 

C. W. Suckling. “ Insanity cared by a New Method.” Comich Brothers, 
Ltd., Birmingham, 1907. 2s. 


will be held at Amsterdam on the 2nd to 7th September 1907, under the 
patronage of Her Most Gracious Majesty Queen Wilhelmina and of His Royal 
Highness Prince Hendrik of the Netherlands. The Congress will be divided 
into two parts: General Sessions and Meetings of Sections. In the former, 
chosen subjects will be dealt with by competent men who have been invited 
for that purpose ; in the latter, questions will be discussed and criticism will 
be invited. Anyone taking an interest in Psychiatry, Neurology, Psychology, 
and the Nursing of Lunatics may become a member of the Congress. Those 
wishing to attend the Congress are requested to communicate with the General 
Secretary, Prinsengracht 717, Amsterdam. 



fleurolOQE anb flbs^cbtatrp 

Original articles 


By J. S. FOWLER, M.D., F.R.C.P.E., 

Physician, Royal Hospital for Sick Children, Edinburgh. 

During the past winter, and particularly within the last two and 
a half months, a number of cases of meningo-coccal cerebro-spinal 
meningitis have been admitted to the Sick Children's Hospital— 
5 under Dr Melville Dunlop, 7 under Dr Thomson, and 7 
under myself. Four cases have also come under observation 
outside the hospital, making 23 in all. Post-mortem examina¬ 
tions have been made by Dr Stuart M‘Donald on 14 of these 
cases, as well as on a number of others not seen during life. The 
following paper 1 is based on this material ; the clinical notes 
refer chiefly to my own cases, though I have to thank my 
colleagues on the hospital staff both for their kindness in allowing 
me to examine patients under their care, and for permission 
to refer to them here. Within the same period 3 cases of 
pneumococcal meningitis have also been in the wards; these 
will be alluded to mainly for comparison. 

Ages and Sexes of Patients, Dates of Onset , and Distribution. 
—The patients comprised 16 males and 10 females ; their ages 
ranged from thirteen weeks to four years. Two of the pneumo¬ 
coccal cases were fatal; one is still alive, and apparently 

1 This paper forms part of a communication read at the Edinburgh Pathological 
Club on March 13, 1907, by Dr Stuart M A Donald and the author. The pathological 
aspects of the disease will be dealt with by Dr M'Donald in a future article. 

R. OF N. & P. VOL. V. NO. 4— R 



improving slightly at the fifteenth day. Of the meningo-coccal 
cases 19 died, 4 remain alive. No patient has yet recovered 
completely. Twelve of the 19 fatal cases terminated in nine 
days or less ; 7 lived from periods of from eleven to forty-seven 
days; in two-thirds of the patients, therefore, the course was 
acute, in one-third chronic. As the table shows, the tendency 




Date of Onset 








Oct. 4 

2 Days 





„ 19 

11 „ ) 





Nov. 28 

36 Hours 





Dec. 14 






Jan. 5 

5 Days 





„ 5 

24 „ 





„ 6 






„ 10 

47 Days 

. 8 




„ 20 

29 „ 





„ 22 

82 Hours 





„ 23 

9 Days 





„ 25 

11 „ 





„ 27 

17 „ 




F 1 

„ 30 

21 „ 





Feb. 9 

56 Hours 





» 9 

9 Days 





„ 10 

4 ) 





„ 20 

26 Days 





„ 22 

4 „ 





„ 25 

5 „ 





„ 26 

Still living) 





„ 26 

80 Hours 





„ 27 






„ 27 

38 Hours 







5 Days 





Mar. 4 


a — Pneumococcal meningitis. 

latterly has been towards the preponderance of the more acute 
type, for during February we had not so many protracted cases 
as in January. The cases have been scattered all over the city ; 
we have had cases from the old town, the southern suburbs, the 
Dairy and Gorgie district, Greenside and South Leith, and the 


north side of the town. They have not been limited to the 
poorest localities. With one possible exception, to be mentioned 
later, no two cases have occurred in the same house or family. 
Even when cases have occurred in adjoining localities, -a 
considerable interval of time has often elapsed between them. 
The parents of the affected children have followed a great 
diversity of occupations, and it has not been possible to trace 
any common source of infection in this quarter. There has 
been no apparent connection between the incidence of the 
disease and the mean temperature. 

Clinical Features. —I do not propose to give the detailed 
analysis which has been made of the clinical features of these 
cases; but only to draw attention to what was made out as to 

(1) the antecedents; (2) the onset; and the leading symptoms, 
(3) head retraction and rigidity of the back ; (4) the reflexes 
and other nervous symptoms; (5) lumbar puncture; (6) 


(1) Antecedents. —Most of the patients were in good health, 
and were well-nourished children. One had suffered from a sore 
throat the week before, and one had a definite history of a fall 
on the back of the head three days prior to his illness. There 
was no nasal or ear disease. No case occurred in an exclusively 
breast-fed infant. One of the pneumococcal oases had otorrhoea, 
another, an abscess in the arm, at the date of onset. 

(2) Onset. —The outstanding feature was its suddenness. 
In many instances, the exact hour of invasion was known. To 
give an example : a little boy was out playing until 7 o'clock 
one evening, and came home to supper and went to bed as 
usual. At 3 a.m. he awoke delirious, with pains in the back 
and head, and died within fifty-six hours. Fever is invari¬ 
able, and next in frequency comes vomiting, which may continue 
during the. course of the disease. An initial convulsion occurred 
twice, and a history of headache was given by all but one of the 
patients over two. It was never severe, and was not often 
complained of by patients in hospital. Very often some 
Blight cerebral symptom, such as a dazed, staring look, was 
spoken of. On the whole, except for its abruptness, the in¬ 
vasion of cerebro-spinal meningitis is not unlike that of any 
other acute infection. 

(3) Rigidity of the Back and Head Retraction. —One or both 



of these was present in every case at some period or another. 
Our previous experience of these was based on what we are 
accustomed to see in posterior basic meningitis, and from this 
point of view, neither (taking the cases as a whole) was as 
constant and striking a feature as was anticipated. Both are 
most marked in the protracted cases, in which they may become 
extreme, the patient boring the head into the pillow so that 
the occiput rests between the shoulder blades (Fig. 5 and 6). 
In acute cases they are often so slight as readily to be over¬ 
looked, especially in young infants (Fig. 1). There may be 
nothing more than a little resistance to movements of the head 
and neck, or the fact that attempts to do so cause crying. In 
two patients, one an acute, the other a chronic case, neither 
sign was present on admission on the first and the eleventh days 
respectively ; in two of the most acute cases, which lasted for 
only thirty-eight and fifty-six hours, all that was ever present was, 
in the one, transient slight stiffness of the back, in the other, 
crying when the head was bent forward. In only three patients 
were stiffness and head retraction marked on admission. The 
earliest date at which definite permanent arching of the back 
and retraction of the head set in was the eighth day; the latest 
were the thirteenth and twenty-second days. In their classic 
form, then, the symptoms belong to the second week. Some¬ 
times the head retraction preceded rigidity of the spine, 
sometimes vice versd. 

4. Reflexes, etc .—The knee-jerks were abolished in 3 cases, 
doubtful in 1, and active in 4. They were never distinctly 
exaggerated in the meningo-coccal cases, but in the pneumo¬ 
coccal cases they were, once with ankle clonus. The plantar 
reflex was absent thrice; in the others it was flexor. The most 
interesting feature concerning the reflexes was observed in 
connection with the abdominal reflex, which was abolished in all 
the meningo-coccal cases (see foot-note, p. 257). As a rule, this 
reflex can be elicited even in young children if the abdominal 
parietes are relaxed, and to the question of its absence we shall 
revert later. Kernig’s sign (Fig. 4) was absent on admission in 
6 cases, and in 3 of these it was never developed; in the rest 
it was fairly distinct. It may be quite obviously present even 
in young infants with flabby muscles. Thus it was noted as well 

Plate 9. 

Fig. 1.—Case 8. Purulent cerebro-spinal fluid. Absence of 
head retraction at onset. 

Fig. 2.—Case 8. Development of head retraction towards end 
of illness. 

Fio. 3.—Case 20. Slight head retraction. Swelling of left knee-joint. 

Plate 10. 

Fig. 5.—Case 13. Condition on day before death. Note opisthotonos, 
rigidity, and }>osition of fingers and toes. 

Plate 11 

tram from Case 7, showing patches of exudation over 
cerebellum and pons. 



marked on the 3rd day in an infant aged 9 months, and it may 
occur from the onset. 

Among other nervous symptoms, tremors and jerkings of the 
limbs, mostly of small amplitude, occurred in about half the 
patients. One child had a curious alternating hemispasm, in 
which first the left arm and leg began to jerk; after a quarter of 
a minute or so this ceased, and then the right arm and leg 
began. The cycle was repeated every 3 or 4 minutes for 
several hours. In other cases tremors were a terminal symptom. 
Paralyses of the limbs were absent. One infant was during her 
whole illness in a condition of general spastic rigidity—arms 
flexed, hands clenched, legs extended and adducted, toes turned 
in to soles. She presented a phenomenon the reverse of Kernig’s 
sign, viz., when the leg was flexed at the knee it tended to spring 
back to the extended position as soon as the pressure was 

Mental Condition .—As a rule, patients are apathetic when 
unmolested; hyperaesthetic if disturbed. One was actively 
delirious, climbing about his cot whenever he was left alone. 
One could not but be struck by two circumstances: first, that 
considering the gravity of the malady, the patients expressed 
so little sign of pain; second, that consciousness was so well 
preserved, notwithstanding the presence of acute inflammation 
of the meninges. A boy of 4, whose illness lasted just two days, 
could sit up and answer questions perfectly clearly 18 hours 
before he died; a baby of a year smiled and played quite con- 
tentedly; a girl of 4 used to sing happily to herself. The two 
last were chronic, though fatal, cases. 

5. Lumbar Puncture. — The meningo-coccus was always 
detected without much search in the cerebro-spinal fluid, although 
sometimes we failed, for no obvious reason, in first attempts to 
get fluid for examination. The organism was found throughout 
the whole course of the malady except in two instances, in which, 
after the 12 th and 22 nd days respectively, it could no longer 
be detected. The fluid always contained many polymorpho¬ 
nuclear leucocytes. While lumbar puncture is chiefly of 
importance as leading to a correct diagnosis, to which end it is, 
of course, essential, it is worth while inquiring whether the 
information derived from it (1) is of any value in estimating the 
probable duration of a case, (2) has any bearing on the clinical 

254 J. 8. FOWLER ' ’ 

features, and (3). whether; the procedure is of any use thera¬ 
peutically. i 

(1) Lumbar Puncture and the Duration of the Illness .—In the 
most acute cases, lasting only a few days, the fluid was milky or 
moderately turbid, and dropped out freely—never flowed from 
the cannula in a continuous stream. In some chronic cases it 
was much the same. The least turbid, almost purely serous 
fluid, which spurted out under high pressure, came from a 
chronic case. In the two most protracted cases the fluid was 
either purulent from the first, or became so later on; in both 
instances only a small quantity was obtained. The number of 
organisms found bore to some extent a relation to the acuteness 
of the case. In very acute cases they may be scanty, and in 
chronic ones they may be comparatively few. On the whole, in 
moderately acute cases they are most abundant. They were 
always found both in and outside the cells. In the most acute 
case observed (38 hours) very few were intra-cellular. Speak¬ 
ing generally, then, it may be said that turbid fluid under 
moderate pressure, swarming with organisms, betokens a bad 
case ; few organisms, with severe constitutional symptoms, mean 
a very acute infection ; while few organisms, with mild symptoms, 
mean a less severe attack. Serous or purulent fluid alike point 
to a protracted course. 

(2) Lumbar Puncture in Relation to Symptoms .—We expected 
to find some sort of relation between the character, and 
particularly the pressure, of the cerebro-spinal fluid, and the 
presence or absence of such symptoms as Kemig’s sign, spinal 
rigidity, etc. No such relation, however, seems to exist We 
must recall the fact that intra-spinal pressure, as shown by the 
rate of outflow, is not an absolute index to what exists inside the 
cranium, because in chronic meningitis, matting at the base of 
the brain readily blocks the channels between the cranium and 
spinal canal, and may even lead to hydrocephalus without there 
being any rise in the intra-spinal tension. Here, however, we 
are concerned only with the pressure uilder which the cerebro¬ 
spinal fluid escaped on lumbar puncture. Of 2 cases in which 
there was no rise in pressure, one had rigidity of the spine and 
increase of the deep reflexes to a more marked degree than any 
other patient; the second had neither. Of 5 cases with , turbid 
fluid under pressure, 2 had marked stiffness of the back, 3 very 


little. In another case, in which the pressure,, ftt first very high, 
fell steadily, head retraction and opisthotonos developed in 
almost inverse ratio. In that patient a good deal of matting 
was found post-mortem about the base. Pressure, therefore, as 
shown by the rate of outflow, does not appear to influence the 
symptoms much. , 

(3) As regards the Therapeutic Effect of Lumbar Puncture, the 
general impression gained from watching the cases was that it is 
small In my own series of cases it was done about 40 times 
for diagnostic purposes and for treatment. One acute case, in 
which on 5 occasions within 36 hours about 6£ ozs. of fluid 
was withdrawn, was invariably relieved for the time being by 
tapping. In another case head retraction diminished consider¬ 
ably, but only for about 4 hours, after removal of cerebrospinal 
fluid. Apart from these two instances, no benefit was obtained. 
On the other hand, two patients became temporarily collapsed 
after the withdrawal of small quantities. Wc: were guided as to 
the amount drawn off by the rate of flow and the aspect of the 
patient; if there was no distress the cannula was left in position 
until the fluid ran less freely. In pneumococcal meningitis no 
good followed puncture. , 

Intra-spinal injections of 1 per cent, lysol and of collargpl 
were tried without avail. The former had no apparent effect 
one way or another. The latter gave rise to unpleasant 
symptoms, such as tremor and violent delirium, on several 
occasions. More important, however, from a practical point of 
view, is the fact that on post-mortem examination of a patient 
who was under treatment with collargol, indisputable traces of 
the drug, which has a dark-brown colour, were found in. the 
exudate at the base of the brain. It is therefore reasonable 
to suppose that injection of a suitable antiseptic might be of 
value in treatment. 

6. Rashes .—Two forms of rash occur : herpes and purpqra 
or erythema. The characters of the latter vary greatly. In 4 of 
the 8 cases there was no eruption whatever. Four, at least,, of 
our hospital cases—3 chronic and 1 acute—-have had well- 
marked labial herpes as an initial symptom; there has been no 
instance of its occurrence in any other region. A true haemor¬ 
rhagic rash was present in two cases in hospital and one outsider- 
all of them acute. In one the whole body was covered with 



purpuric spots, varying in size from a pea to a threepenny piece, 
with a large extravasation over the knee-joint. In a second case, 
on the morning of admission (second day), the rash consisted of 
reddish-purple macules, sparsely scattered over the chest and 
arms, not unlike commencing measles or the earliest appearance 
of chickenpox. In the evening the rash had become much more 
profuse, but still retained its erythematous character. Next 
morning most of the spots had faded; a few had become 
hemorrhagic, and persisted till death. In several patients 
evanescent mottling, chiefly about the extensor aspects of the 
arms, was noted. This seemed to be connected with a tendency 
towards cyanosis which exists in cerebro-spinal meningitis. The 
patients were often slightly dusky on admission, and became 
very livid towards the end. The impression it gave was that it 
was due as much to toxsemia as to malaeration. In most cases 
the blood was examined. There was always a leucocytosis 
(14,000 to 38,000), and usually a positive glycogen reaction. 
In the case with serous exudation, the latter was absent 

Relation of Epidemic Cerebro-Spinal to Posterior Basic Menin¬ 
gitis. —Simple basal meningitis is a well-known, not very un¬ 
common disease of children. Fifty per cent, of the patients are 
under 6 months, 84 per cent, under a year, and 90 per cent 
under 2 years. It is therefore a malady which almost solely 
affects young infants. It runs a chronic course of seven weeks 
on the average, and is not always fatal. Dr G. F. Still has 
described a diplococcus, almost identical with the diplococcus 
intracellularis meningitidis, which has since been constantly found 
in the cerebro-spinal fluid in the disease, and most authorities 
now regard posterior basic simply as a sporadic form of epidemic 
cerebro-spinal meningitis. We were, therefore, especially in¬ 
terested in comparing the cases we have lately seen with those to 
which we were formerly accustomed. The acute disease is, of 
course, totally different clinically. Chronic cases, however, are 
so very similar in many respects, that it is impracticable to draw 
any hard and fast line between the two conditions. At the same 
time, there have been minor peculiarities. Taking the chronic 
cases as a whole, it may be said that almost any one of them, 
had it occurred alone, would have been looked on as a rather 
aberrant type of posterior basic meningitis. For one thing, many 
of the patients were of an age at which posterior basic meningitis 


is rare. Again, meningo-cocci were, on the whole, more abundant 
in the cerebro-spinal fluid, and there were more intracellular 
forms. A notable point of difference was the existence of labial 
herpes in three or four cases. According to Barlow, this is very 
rare in posterior basic meningitis—indeed, he comments specially 
on the fact as remarkable, considering the close relation of the 
disease to the epidemic form. There is no doubt that posterior 
basic is a sporadic variety of epidemic meningitis, but it seems 
as though, when an epidemic prevails, the organism undergoes 
modification, so that it no longer tends specially to affect children 
under a year, or to reproduce exactly the same symptom-group 
which it does in common sporadic cases. 

Relation of Cerebro-spinal Meningitis to Acute Abdominal In¬ 
fection .—The suggestion that epidemic cerebro-spinal meningitis 
may be related to acute abdominal infection originated primarily 
from certain pathological observations made some months ago by 
Dr Stuart M'Donald, to whom the credit of priority is therefore 
due. For the sake of clearness, however, the pathological as 
well as the clinical facts which appear significant are stated 
here; the former will be elaborated by Dr M'Donald in a future 

The commonly accepted etiology of cerebro-spinal meningitis 
is that the organism gains access to the brain from the nasal 
cavity. Without denying that this may occur, we can only say 
that we found neither clinical nor pathological evidence support¬ 
ing it. There seem, however, to be certain facts tending to show 
that in cerebro-spinal meningitis the cord lesion is primary, and 
that the diplococcus invades the nervous system through the 
spinal meninges. 

1. In most cases the post-mortem appearances show that 
the cord lesion is of older standing than that of the brain. 

2. The constant early and complete abolition of the abdominal 
reflex, already referred to, seems to point to early implication of 
the lower dorsal cord. 1 It is interesting to compare the pneumo¬ 
coccal cases (in which the lesion is primarily cerebral) in this 
particular. In one of them the reflex was active. Lumbar 

1 Since this paper was written, I have observed the abolition of the reflex in 
several other cases, and its return in three cases daring convalescence. In one acute 
esse I have also found it to be present, but the general rule that the reflex is absent, 
does not seem to be invalidated by this single exception. 



puncture, a few days before death, yielded clear fluid, with no 
cells or organisms. In the second and third cases the fluid was 
turbid, and swarmed with pneumococci; in them the reflex was 
absent. It is therefore justifiable to conclude that the abolition 
of the reflex points to spinal lesion. The withdrawal of clear 
sterile fluid from a case of pneumococcal meningitis is noteworthy. 
Osier states that a negative finding of this kind is common in 
such cases, so long as the meningitis remains limited to the 
cranium. If this be so, the fact that meningo-cocci can be detected 
in the fluid in cerebro-spinal meningitis from the very onset 
is an additional argument in favour of the spinal origin of the 

3. Another small fact, tending, however, in the same direc¬ 
tion, is the slight amount of disturbance of cerebral function in 
some of these cases. The retention of consciousness late in the 
disease has been mentioned; a child may be able to sit up quite 
contentedly days after pus has been removed from the spinal 
canal. (Fig. 1.) 

If, therefore, as there seems some reason to suppose, the 
brunt of the infection first falls on the cord, the most natural 
channel of entry is from the abdominal cavity. The information 
bearing on this is for the mogt part pathological; but two pieces 
of clinical evidence may be given. 

4. A possible exception to the statement that no two cases 
occurred in one family, has been spoken of. A child died of 
acute cerebro-spinal meningitis on a Friday morning after 2 days' 
illness. On Sunday an infant sister, aged 3 weeks, died after 
12 hours’ illness. She was seen by the same student who 
had recognised the nature of the first case, and was supposed 
merely to have some digestive disorder. Post-mortem, the brain 
and cord seemed healthy; the appearances in the abdominal 
cavity were similar to what are seen in many cases of cerebro¬ 
spinal meningitis, and the diplococcus meningitidis was found in 
smears made from the base of the brain. 

5. No case of meningo-coccal meningitis in an exclusively 
breast-fed infant has come under our notice. The possibility 
of bowel infection is therefore evident. In the case just referred 
to the infant was nursed until the elder child took ill, when the 
mother’s milk failed. During the last four days of life, therefore. 


and for three days preceding her illness, she, also, was fed 
artificially. , 

Finally, I may again emphasise the fact that lumbar puncture 
is of paramount importance in regard to diagnosis. In very 
acute cases, in children at least, the characteristic symptoms 
may be so slight at the onset, that even after some little experi¬ 
ence of the disease, one remains in doubt until the cerebro-spinal 
fluid has been seen. The procedure is safe and easy to carry 
out, and the withdrawal of a little turbid fluid suffices practically 
to clear up the nature of the case. 


Physician to Leith Hospital. 

The condition of stammering, though not exactly common, 
occurs amongst all classes with a frequency that deserves, J. 
venture to think, a more adequate recognition from the medical 
profession than it generally receives. That the fault lies 
entirely with medical men I do not, of course, maintain; for 
few things are more striking than the acquiescence of th,e 
parents or relatives of a stammerer in regarding his malady 
as only “ a bad habit,” or “ largely the result of nervousness 
a matter, therefore, in their opinion, on which medical advice 
need not be sought. Now, this fact (and it will be generally 
admitted, I think, that a doctor is seldom consulted upon the 
subject of stammering) is of much interest. For every general 
practitioner knows well the eagerness with which his advice 
is sought (and his “ operative ” assistance often urged) by an 
anxious mother who imagines her infant (of a few weeks) 
to be “ tongue-tied ”; and yet when, in later years, one (or even 
more) of the children in 'a family shows even marked stammer¬ 
ing, the family practitioner is rarely consulted on the matter. 
Relatives and friends, more or less sympathetic but probably 
all equally ignorant of the subject, may be spoken to about 
the boy*8 infirmity, or the advice even of the clergyman may 



be sought, but the family doctor in such a case is too often 
looked upon as a dernier ressort. 

Or, again, should one of her children show signs of “ limp¬ 
ing ” or “ halting ” in his gait, no time is lost in seeking the 
advice of the medical attendant, who is closely questioned as 
to the possibility of any incipient joint disease; and yet another 
little sufferer—perhaps partly because his pain is mental rather 
than physical, and so does not betray its presence by fretful 
crying—is frequently allowed to go on for years “ limping ” in 
his speech, developing an increasing “ impediment ” which may 
cripple his whole after-life. At the door of the stammerer’s 
relatives, then, a goodly proportion of the blame for the neglect 
of this serious affection must undoubtedly be laid. 

But, on the other hand, does it not too often happen that, 
should the advice of a doctor be sought regarding a stam¬ 
merer, he is rather at a loss as to how the condition should 
be treated. And yet the fault is not mainly his, for the subject 
was very probably not dealt with at all in his undergraduate 
teaching, and to his usual text-books he will turn almost in vain ; 
for although in some of the larger cyclopaedias or “systems” 
of medicine of recent years the question is considered, the 
affection is scarcely mentioned in the ordinary text-books. 
Hence it may not be altogether without reason that, in dealing 
with such an affection, it has been customary on the part of the 
public to reckon the family doctor’s advice as only secondary in 
importance to that of the boy’s school-teacher or clergyman, who 
are both regarded as more experienced in the management of the 
“ unruly member.” Lack of practical knowledge of the subject, 
then, on the part of the medical attendant, as well as indifference 
of the patient’s relatives, probably account for the comparative 
neglect of the treatment of this important and too common 

The result of this ignoring, to a large extent, of stammering 
by the medical profession, is only too clearly shown by the 
frequency with which one notices in the press advertisements 
of so-called “ cures ” for stammering. There is evidently a 
demand for treatment; is it satisfactory or creditable that our 
profession should concern itself so little with the proper scientific 
treatment of the defects of such a manifestly physiological act 
as speaking? 


Nov it is worth noting that, while the methods of some 
of those so-called “stammer doctors” pertain largely to pure 
quackery, it is undoubtedly true that others have really 
given some attention to the study of the subject, and by the 
adoption of certain modes of treatment (not by any meana 
scientific) have produced sometimes results which are, on the 
whole, fairly satisfactory. Such being the case, one might 
expect that accurate scientific investigation of the subject, 
founded on physiological data, should give still better results. 
The treatment of a neurosis (such as stammering undoubtedly 
is) ought not to be considered as outside the domain of the 
medical profession. No small part of the curriculum of the 
student of medicine is taken up with instruction—systematic 
and clinical—in nervous ailments, organic and functional. Why 
should the study of stammering be so neglected ? I have heard 
it stated that a medical man might be apt to be regarded 
as dabbling in quackery should he become known as qualified 
to treat cases of stammering. Can this be another explanation 
of the comparative neglect of the subject by neurologists and 
medical teachers generally ? There can, I think, be little doubt 
that the ignorance of the practitioner on the treatment of thia 
too common affection must really be laid at the door of his- 

Surely the family medical attendant ought to be as 
competent to give advice as to the rectification of faulty 
speaking as he is in the correction of faulty walking, e.g. in 
incipient “ flat-foot ”—an instance where accurate study of the 
anatomy of the foot revealed clearly the muscular exercises 
which are likely to strengthen and develop the faulty supports 
of the plantar arch. Now, undoubtedly "flat-foot” is a con¬ 
dition which comes under the notice of medical men much more 
than stammering, but if the seriousness of a malady is to be 
measured, not by the frequency of its occurrence, but by the 
amount of suffering it entails, I venture to maintain that in 
the stammerer we have a patient deserving of our utmost 
consideration. Probably few, except those who have been its 
victims, can realise the amount of mental suffering endured 
by many stammerers—not merely the fear of ridicule in boy¬ 
hood, but the attendant nervousness and actual difficulty of 
enunciation of many school lessons, e.g. many Greek verbs 


Wit!h their reduplicated voiceless consonants (e.g. titto, vtrrvxa). 
The nervousness which is so often assigned by the patient’s 
friends as a cause of his affection is much more truly one of 
its results ; another of which, in many instances, is a morbid 
shyness and avoidance of company on the stammerer’s part. 

Granting, then, the importance of the subject of stammering 
abd the need for its more systematic treatment by the medical 
profession, how can this be undertaken ? I desire to draw attention 
to the method of treatment advocated by Prof. Wyllie of Edin¬ 
burgh University, in his articles which originally appeared (in 
1891) in the Edinburgh Medical Journal, and were subsequently 
published in his work on “ The Disorders of Speech.” As one 
of hie earliest pupils when he was working at the subject, I have 
long since proved the great value of his teaching, not only 
by my own personal experience, but also by putting his methods 
into practice on others. I have previously endeavoured 1 to 
enlist a wider interest on the part of the profession in Wyllie’s 
Method, and drawn attention to its comparative simplicity; for 
the value of his admirable work is, to a considerable extent, I 
think, lessened by the fact of its being contained in a work 
on a special subject which rarely finds a place on the shelves 
of the general practitioner. Now, his method of treating 
stammering is essentially designed not merely for the specialist, 
but for the practitioner, who can carry out the treatment of 
the condition satisfactorily in the most outlying country village, 
provided —and this is the crux of the whole situation—the 
patient will perseveringly carry out the instructions given. 
Stammering is one of those conditions to the treatment of which 
the old adage is especially applicable about taking “a horse to 
the trough,” etc. It is the patient who must carry out per¬ 
sistently (under medical supervision) the instructions laid down 
for him, and it is on his own perseverance that the rapidity 
and completeness of his cure will depend. 

Those who desire a fuller exposition of Wyllie’s views, 
not merely on stammering but also developmental affections 
of speech, will find them in his book (“ The Disorders of 
Speech ”); my endeavour here will be to give a r4sumd of his 
treatment of stammering, with some additional notes on certain 

1 Brit. Med. Journal , July 20, 1901; Practitioner, January 1903. 


Symptoms. — No detailed account of the symptoms of 
stammering is required, but there are, of course, many varieties 
of the condition ; these, however, fall into two main groups: 
(a) those who “stutter,” i.e. show a tendency to the rapidly 
recurring enunciation of the particular letter-sound which has 
caused the difficulty in speech; ( b ) those who (in Wyllie’s 
phrase) “ silently stick ” at the difficult letter. The first variety 
(who say, e.g. “p-p-poor B-B-Bob”) is found more commonly 
open the dramatic stage than in real life. The patient with 
the other and commoner variety tends (as Wyllie says) to 
manufacture a “great big capital” P (in saying “Poor Bob”), 
instead of several little “p’s,” the process of the evolvement 
being generally silent (hence the unsuitability of this type for 
representation on the stage). But though there is practically 
nothing audible to the bystander during' the interruption of the 
patient’s utterance, very frequently other evidences of the 
stammerer’s distress and difficulty can be seen (congestion of 
the face, grimaces, etc.), which are well described by Kussmaul. 
These involuntary facial and other movements should be dis¬ 
tinguished from certain purposive actions ( e.g. tapping with 
the foot, swaying of the body, etc.) sometimes made use of by 
patients who have found from personal experience, or having 
been taught by a “ stammer - curer,” this muscular outlet 
helpful in overcoming their difficulties. It is, of course, well 
known that it is especially initial letters that cause trouble to 
stammerers; that consonants are far more frequently a source 
of difficulty than vowels ; and also it is where using the ordinary 
conversational tone that stammering is apt to be worst. The 
condition is much more common in the male sex at all ages. 
Most important of all is it to note that scarcely ever does a 
patient stammer in singing. 

Pathology .—This requires only the briefest notice. Stam¬ 
mering is essentially a functional affection—a neurosis the result 
of defective working of the complex co-ordinated mechanism 
concerned in the production of speech, and not a defect of 
structure. Pathological lesions, therefore, connected with it 
cannot be looked for, and herein lies one of the great induce¬ 
ments to the adoption of proper scientific treatment of the 

Treatment. —In each of the two classes of stammerer men- 



tioned above, the difficulty of enunciation will be found to be 
essentially due to a want of the necessary harmony between the func¬ 
tions of vocalisation and articulation. The first essential, then, in 
commencing treatment of any case is to explain to the pupil 
briefly the process of normal speech utterance. It is not 
necessary to take him at any length into the physiology of the 
subject, but he must be made to grasp clearly the fact that 
during the act of speaking three separate mechanisms are 
harmoniously at work: (1) a current of air is being expelled 
from the lungs; (2) sounds are produced in the larynx ( vocalisa¬ 
tion) by the vibration of the vocal cords; (3) these initially 
laryngeal sounds (and others also, as will be seen later) may 
be modified by the actions of the lips, tongue, etc. (articulation). 

The great value of the first of these co-ordinating mechanisms 
will be alluded to subsequently; what the stammerer has to 
grasp is that his difficulty is essentially due to defective co¬ 
operation between vocalisation and articulation , and in by far the 
largest number of instances it will be found that it is his 
vocalisation which is at fault—being deficient in amount as 
well as in promptitude. The simile which Wyllie makes use 
of to illustrate this appeals at once to any pupil. He compares 
the co-ordinated mechanism at work in speaking to the perform¬ 
ance of a violinist: just as the player’s right hand (“ bow hand ”) 
produces sounds which are modified into notes by the left 
(“ string hand so (in speaking) vocalisation corresponds to the 
“ bow hand ” and articulation to the “ string hand.” Now, we have 
seen that it is the stammerer’s vocalisation which is faulty in 
the greatest number of cases—being lacking both in volume 
and promptitude—and he usually attempts to make up for this 
deficiency by excessive articulatory efforts. Any lay pupil can 
be got to see that just as a violinist would utterly fail to produce 
any music from his instrument if, neglecting his bow hand , he 
puts his misdirected energy into the string hand, so the stammerer, 
forgetting the essential vocalisation , must inevitably “ stutter ” or 
“stick” in his attempts to produce words by (exaggerated) 
articulation alone. He can thus be got to realise that he stam¬ 
mers because he bestows too much attention upon articulation and 
too little upon vocalisation ; the main object, then, in treatment is 
to emphasise and bring out whenever possible the vocal element 
in words. 


The real significance of the fact (previously mentioned) that 
practically no one ever stammers in singing is thus revealed to 
the pupil, who has usually noted the fact for himself without 
understanding the reason. It is just because in singing vocalisa¬ 
tion must be emphasised (and the full vocal value given to words) 
that articulation presents no difficulty to the stammerer. It is 
well at the first lesson, then, by insisting on this characteristic 
feature in stammering, to endeavour to inspire the pupil with 
confidence in his ability to conquer his difficulty even in ordinary 
speaking, if he will learn how all-important vocalisation is. 

It may be of some interest to mention here another instance 
of the practical value of emphasising the vocal element in words 
which was discovered by the writer many years ago. He found 
that the pronunciation of many well-known stumbling-blocks 
presented practically no difficulty if the “ voice ” or “ tone ” of 
someone else was made use of during their enunciation ; the 
stammerer’s attention was so directed to the production of the 
correct sound that the articulation of the difficult words was as 
easy as in singing. As pointed out elsewhere, 1 this little “ tip ” 
may be useful in many cases (to those stammerers who have the 
faculty of imitating the voice of others) by enabling them to read 
aloud (should they be asked to do so) before strangers, who 
probably will not be aware that the reader is making use of 
any other than his own natural voice. 

The great importance of attention to vocalisation by the 
stammerer having been sufficiently insisted upon, the pupil 
should next be taught how to deal with the different letter- 
sounds which present difficulties to him. For the purpose of 
tabulating this, Wyllie has drawn up what he terms a Physio¬ 
logical Alphabet, a copy of which, by his kind permission, is here 

1 The Practitioner, January 1903* 





I. Vowels. 

Y—I E A O U—W 

These should be pronounced in the Latin manner as ee, eh, 
ah, oh, 66; y and w are consonants, not vowels, but are placed 
here for reasons given in the text. 

II. Consonants. 

Voiceless Oral 

Voiced Oral 

Voiced Nasal 


(First Stop-Position) 










Th 1 




(Second Stop-Position) 









(Third Stop-Position) 


H or Ch 





The voiceless W and voiceless L have been shown in brackets, 
the former being now almost confined to Scotland, the latter 
being peculiar to Wales. The uvular (burring) R is also put 
in brackets. 

It will be well to indicate the main features of his plan in 
drawing up this alphabet, beginning with the first group of 


I. Vowels. 

Since all the vowels are essentially produced in the larynx, 
and are thus full of “voice,” they are not grouped in columns 
as are the consonants. The pupil should be instructed to give 
the full vocal emphasis to each of them in speaking, but as a 
general rule it will be found that the vowels are not a source 
of difficulty to stammerers. Wyllie’s reason for placing the 
two consonants W and Y along with the vowels is interesting, 
especially to stammerers. It so happens that words commenc¬ 
ing with either of these two letters prove very frequently a great 
source of trouble to pupils who attempt to pronounce them 
voicelessly, the air escaping fruitlessly from their lips. Now, 
each of them is essentially a voiced letter (as shown in the table 
of consonants), but further, Wyllie points out that an initial 
W is really (when considered phonetically) equivalent “to a 
tight do with a slight fricative element added,” Y being similarly 
equivalent to 66 with a slightly fricative addition. Thus the 
words “ will you ” might be phonetically spelt “ 06 -ill 66 -ou,” 
the resemblance to the pure vowel sounds being so great that 
W and Y may be regarded (as Wyllie suggests) as “ stepping- 
stones ” between the vowels and consonants. Now this is not 
merely a matter of interesting speculation ; for the stammerer 
it gives a lesson of the greatest value. Many very common words 
have these letters for initials, and the word “ yes ” alone plays 
a great part in conversation, and yet it is extremely common 
to find the stammerer having marked difficulty with it because 
of his attempts to pronounce the initial letter-sound voicelessly 
as ** yeh.” Get the pupil to grasp the fact (and prove it to himself 
by practising) that the word “yes” can be (and should be by 
him) pronounced almost as if in two syllables—“ ee-ess ” (with 
ample vocalisation of the initial 66 ), and he will find he has not 
only got over this oft-recurring stumbling-block, but obtained 
the key to the enunciation of a whole host of formerly trouble¬ 
some words, his guiding rule being essentially this, viz.: all words 
having an initial Y to be pronounced as if they began with 66 ; 
all beginning with W (except those commencing with “wh”) 
to be pronounced as if commencing with 66 . 



II. Consonants. 

It must be noted at the outset that each of these is con¬ 
sidered in the alphabet “ as it is pronounced during the enuncia¬ 
tion of a syllable containing it ”; e.g. F is regarded, not as “ eff,” 
but the initial sound in a word (“ fat ”). 

The great importance of recognising the vocal element in the 
consonants is shown by the manner in which Wyllie separates 
“ voiceless ” from the “ voiced ” letters. This is the essentially 
important feature in the arrangement of the alphabet so far as 
concerns the stammerer; the horizontal grouping of the letters 
by Wyllie does not concern us in this article, though of no little 
importance in other respects. 

It is most important that the pupil should be made to prove 
to himself (by practising) the fact that, while the larynx takes 
a very prominent part in the enunciation of each one of the 
consonants grouped in the second and third columns of the 
alphabet, those classed as “ voiceless oral ” have really no 
laryngeal element of “ voice ” in them at all, being produced 
(as the names applied to them indicate) in the oral cavity by the 
action of the lips, tongue, teeth, palate, etc. upon the air expelled 
from the lungs. It is this essential distinction which plays such 
an important part in the training of the stammering pupil, for 
whom the rule (in dealing with consonants) may be thus sum¬ 
marised : In speaking or reading , each of the consonants which 
normally contains “ voice ” must have its full vocal dement given 
to it; those which are normally voiceless should be touched off as 
lightly as possible, the voice being brought out with emphasis on the 
ensuing vowd or voiced consonant. Perhaps this will be best 
illustrated by an example, e.g. in saying “Tom Bowling” the 
voiceless “ T ” is to receive quite a different treatment from the 
vocalised “ B.” The initial T is scarcely to be pronounced at all; 
the pupil is merely to apply such compression to the air in 
his mouth as will communicate an explosive character to the 
fully voiced residue of the word “ -om.” The stammerer’s natural 
tendency is to direct his energy to the initial letter, but this 
being a voiedets one, it is the ensuing part of the word that 
he is to concentrate his attention upon—the smallest possible 
T (as it were) being produced which will suffice to clothe the 
vocalised fragment and convert it into the word “Tom." On 


the other hand, B is a voiced consonant: the pupil must therefore 
throw his voice boldly into its production, emphasising the 
laryngeal element of it, so that it almost sounds as if it were 
spelt “ub-owling.” The pupil thus must learn to touch off 
as lightly as possible the voiceless (one might almost call them 
“ articulatory ”) letters—merely forming them without attempt¬ 
ing to sound them—whereas the voiced initials are to have their 
vocal element almost exaggerated. 

Now, if the teacher will go over seriatim the letters in 
Wyllie’s alphabet he will easily manage to demonstrate to 
the pupils the existence or absence respectively of “ voice ” in 
each, and it is most important that the pupil should be made to 
prove to himself the nature of each (by experiment in his teacher’s 
presence), so that he may be made to realise this all-important 
distinction, and not merely learn off the columns of consonants 
by rote under their respective headings. It is also easy to show 
that the intrusion of “ voice ” into one letter may convert it into 
another,^. if “voice” is added in saying the word “pan,” it 
inevitably becomes ” “ ban,” and similarly D, V, Z, and G (hard) 
are the voiced equivalents of T, F, S, and K respectively. It is 
well worth spending some little time over this important part of 
the subject, for it is upon his accurate knowledge of the nature 
of each consonant (and his compliance with the rule for the 
treatment of each group) that the success of the pupil’s efforts to 
effect a cure will depend. To test his accuracy, therefore, it is 
well at each lesson to ask him to point out in any given sentence 
the first letter in each word on which the voice is to be thrown, 
e.g. t “ Pttt money in thy purse ” (note that “ thy ” is an instance 
of the voiced “ th ” as contrasted with the voiceless “ th ” of 
such a word as “ thin ”). Moreover, the teacher should carefully 
watch during the lessons to see not only that the voiced con¬ 
sonants are properly emphasised, but that the voiceless letters are 
also reduced (as it were) by the pupil to the smallest possible size, 
the correct method of dealing with the particular letter being at 
once pointed out in the event of a difficulty arising. 

As I pointed out elsewhere, 1 the teacher ought to be able (by 
merely listening) to tell whether the letter that the stammerer 
44 sticks ” at is “ voiced ” or not; for if the pupil is giving the 
proper vocal element to each of the voiced consonants, the 

1 Brit . Med. Journal , July 20, 1901, p 31. 



preliminary laryngeal sound will be audible on their pro¬ 
duction. Thus, in saying “ Pepys’ Diary,” the formation of the 
initial letter of the first word is an inaudible act; the explosive 
character of the succeeding letters is silently prepared ; but in the 
enunciation of the next word the pupil should give quite audible 
evidence that a voiced letter is on its way, the laryngeal element 
in the “D”being emphasised as though the word were (phonetically) 
“ ud-iary.” Teacher and pupil thus are to concentrate their 
attention on the differentiation of the voiceless and voiced con¬ 
sonants contained in Wyllie’s alphabet. A few notes upon some 
of the letters (with reasons for certain omissions) may be of use 
in further explanation. 

(1) Voiceless Oral Consonants .—Each of these (in accordance 
with the guiding rule given above), when it occurs as an initial, 
should merely mould the word (give it a shape), so to speak, but 
in no way be allowed to dominate it, the ensuing “ voiced ” letter 
being the part which should receive emphasis. This can be 
demonstrated to the pupil as follows—the viva voce illustration 
being of course much more efficient than the printed words. 
Take such a sentence as “ Fanny took Kate's top,” and teach the 
pupil at first to practise the emphasising of the voiced portion of 
each word, viz. “ -anny -ook -ate’s -op.” When he has grasped 
the need of fully sounding these voiced fragments, let him see 
that the smallest possible enunciation of “ F ” will convert the 
vocalised fragment into the complete word “ Fanny ” ; and so on 
with the others, the voiceless initials are merely to be enunciated , 
the vocalised fragments are to be emphatically sounded. In 
this connection another little “ wrinkle ” may be of some 
service. It is a well-recognised fact that it is especially when 
occurring as initials that the voiceless consonants prove trouble¬ 
some to stammerers. Now, in the sample sentence given above 
it may be seen that the third word (" Kate ”) commences with the 
terminal letter of the preceding word. Since the voiceless K 
has just issued from the pupil's mouth, there is no real need 
for him to reproduce it to “ clothe ” the fragment “ -ate's ” ; he 
merely requires to tack on the terminal “ k ” to the succeeding 
vocalised syllable, as if the sentence ran thus, “ Fanny took-ate’s 
top ”—no pause, of course, to be allowed at the end of the word 
“ took.” This simple procedure, then, may be put thus as a 
working rule : “ When the voiceless initial of any word in a 


sentence is the terminal letter of the immediately preceding word, no 
attempt rued he made to reproduce it as am initial.'’ The practice 
enjoined of “ touching off lightly ” the voiceless initial is thus 
carried to its fullest possible extent, the voiceless initial being 
practically omitted. 

It will be noticed that the letter C does not appear in 
Wyllie’s alphabet—where equivalent to “ soft ” C (as in “ city ”) it 
is represented by S ; where “ hard,” it really represents K (as in 
“ cat ”). WyllieregardsHasa“ voiceless fricative of the posterior 
stop-position,” and certainly on analysing the phenomenon of its 
production it is closely analogous to the terminal soft “ ch ” in 
the word “ loch ” (as a Scot would pronounce it). This is fairly 
well shown by comparing the sound produced by the pronuncia¬ 
tion of the words “ Law he ” with the correct spelling of the 
actual place, viz. “ Lochee.” 

(2) Voiced Oral Consonants. —Sufficient stress has already 
been laid on the need for full vocalisation of each of these, but 
certain letters call for notice. Thus the compound letter-sound 
“ zh ” really represents the sound given to the letter “ s ” in such 
words as “ pleasure ” ; it never occurs as an initial. 

L and R very frequently prove troublesome to a stammerer, 
probably because of the fact that each has a peculiar trilling action 
as part of its articulatory mechanism—in the first case the 
sides of the tongue being brought into play; in the second its 
tip. Here again the pupil is so absorbed with this articulatory 
feature that he usually entirely neglects the more essential and 
primary vocal element present in each; they are both voiced 
fricatives, and must therefore both be thoroughly vocalised. 

The manner in which W should be dealt with (i.e. as “ a 
tight do ”) has been laid down when speaking of the vowels, but 
another important point can be best noticed here. It will be 
found that usually words which commence with two or more 
consonants are particularly difficult of pronunciation by stam¬ 
merers, as if the combination of the two consonantal sounds 
(perhaps one voiceless and the other voiced) overtaxed the 
already defective “ gearing ” of the speech mechanism. Now, 
there are several very common words commencing with “ wh,” 
and it may be well to indicate how these stumbling-blocks can 
be surmounted. The “ w,” of course, represents the vowel “ 56,” 
and is to be sounded as such ; but the pupil must further note 



that in pronouncing such words the “ h ” really phonetically 
‘precedes the “ w,” so that the word “ when ” is to be pronounced 
as if it were spelt (phonetically) “h66-en,” and so with all 
similar words. The stammerer almost always tries to produce 
the initial “ wh ” of such words voicelessly and fails ; let him 
learn to vocalise the “ 56 ” sound of the “ w ” thoroughly (making 
almost two syllables of such words as “ hoo-ich,” “ hoo-ile ”), 
and he will find he can enunciate his former stumbling-blocks 
with ease. In like fashion words commencing with “ tw ” {e.g. 
twenty) and “ sw ” will give no trouble if the “ w ” is fully 
sounded as “ 66,” e.g. “ soo-eep ” (sweep). The importance of 
fully vocalising an initial Y has already been insisted upon. 

(3) Voiced Nasal Resonants. —The letter sound “ ng ” never 
occurs as an initial so no further reference to it is required 
here, but the pupil must have firmly impressed upon him the 
importance of recognising that M and N are each “voiced” 
letters, for it is extremely common to find stammerers trying to 
produce these initial letters voicelessly. Each should be 
produced with a loud emphatic hum (which, as it were, heralds 
the production of the word), so that e.g. the words “North 
Moor ” should be pronounced as if they were spelt (phonetically) 
“ (un)north ” “ (um)moor.” 

A short reference is necessary, before passing from the 
subject of Wyllie's alphabet, to the omission from it of certain 
letters. The absence of C has previously been alluded to; Q 
is unnecessary since it is equivalent to “kw,” just as X is 
in like fashion represented by “ ks ” (compare the sound of 
“ Styx ” and “ sticks ”). The letter J calls for a fuller notice. 
As is pointed out by Wyllie, this is really a compound letter- 
sound equivalent to “ dzh,” which is also the phonetic spelling 
of G “ soft,” as is shown in such a word as “ Jill,” which has 
the exact pronunciation of the Scots measure a “gilL” It is 
very important, therefore, that the pupil thoroughly understand 
that any word commencing with “ soft ” G or J is to be considered 
as commencing really with the letter D, and so must receive 
the ample vocalisation due to that letter. 

In the course of the notes upon the Physiological Alphabet, 
most of the chief difficulties of stammerers have been dealt 
with, but a few more points may be usefully alluded to here 
before summarising the treatment as a whole. The difficulty 


of dealing with two (or more ) initial consonants has been men¬ 
tioned already, but a fuller reference to it here may be helpful. 
When the initial letter is voiceless , and the succeeding consonant 
voiced —as in words like “ train,” “ flow,” etc.—the pupil must 
be taught first to emphasise the voiced portion only, viz. 
“ -rain,” “ -low,” and then practise inserting before these the real 
initial letter of the word, almost inaudibly. For instance, in 
saying such a word as “ proud,” once the pupil has learned the 
need of emphasising the vocal portion (“ -roud ”) he must be 
taught that the very slightest apposition of the lips is all that 
is required to formulate the initial “ p ”—not a tight pursing of 
the lips, as is so apt to be the case with stammerers (with a 
consequent “ bottling up ” of the word in the oral cavity), but 
merely (if the phrase be permitted) the thinnest possible (almost 
diaphanous) garment to clothe the naked form behind it. Still 
more is this minimising of the voiceless initials required when a 
word has occasionally two such letters preceding the voiced 
portion, e.g. “ strike.” 

On the other hand, trouble is sometimes apt to arise in the 
case of words having two voiced initial consonants (as in words 
commencing with “ gl,” “ gr,” “ dr,” etc.), either owing to the fact 
of the stammerer omitting to vocalise the primary initial con¬ 
sonant, or perhaps oftener his attempt to produce the two 
consonants almost simultaneously, with consequent articulatory 
difficulty. He must be taught to throw his voice boldly into 
the primary initial in such words, and usually the remainder of 
the word will then follow easily, containing, as it often does, 
nothing but voiced letters, e.g. “drown,” “gleam.” If such words, 
however, prove very troublesome (as is often the case), then it is 
well (at least in the early stages) to get the pupil to practise 
emphasising the initial letter to such an extent as almost to 
make it a syllable by itself, as if the word were spelt (phoneti¬ 
cally) “ (u)d-rown,” “ (u)g-leam,” etc. 

Enough has been said, I think, to emphasise and expiscate 
the points in the training of the pupil in the use of the Physio¬ 
logical Alphabet. It may be helpful now to summarise the course 
to be adopted in undertaking the treatment of a stammering 
pupil before alluding to one or two final points. 

It is essential at the outset (in his first conversation with 
the pupil) for the physician to notice what is the form of 



stammer manifested by his patient (who will probably, of course,, 
be at his worst under such a nervous ordeal), and in the great 
majority of cases it will be found to present the type described 
above, viz. a lack of amount and promptitude in the vocalisation 
of consonants, with a tendency to exaggerated articulatory efforts,, 
especially in producing the voiceless explosives. 

The first lesson to be given, then, to the pupil is an explana¬ 
tion of the twofold nature of the process in speech-production 
(vocalisation and articulation), and with the help of Wyllie’s 
simile of the violin-player even young pupils can easily be got 
to realise the part played by each of these two functions in 
speaking. Nor is it difficult to get them to realise how greatly 
adequate attention to vocalisation will help them, for nearly 
always these pupils have noticed that they are free from their 
difficulty when singing, so that it is only necessary to explain to 
them the reason of this facility in singing of those words which 
prove so troublesome in talking. Should he be so devoid of a 
“ musical ear ” as to be unable to sing, then occasionally the 
writer’s suggestion as to the adoption of the “ tone of voice ” of 
another may be feasible, in so far at least as to convince him of 
the fact that greater attention to vocalisation (with less attention 
to articulation) is to be his means of conquering his difficulty. 
Another method of demonstrating to the pupil the important 
part played by vocalisation is to get him to read some of the 
sentences of the Prayer-Book in the style and “ voice ” used by 
the Anglican clergy in reading the service. He will nearly 
always be able to enunciate easily in this fashion words having 
initials which cause him difficulty at other times, provided he 
pays sufficient attention to his intoning. Thus, it is well known 
that Charles Kingsley stammered badly in ordinary conversation, 
though able to conduct the service and even preach with little 
hesitancy of speech. Moreover, it must be especially demon¬ 
strated to him that no exaggeration of articulation can ever 
make up for defective vocalisation. Next Wyllie’s alphabet should 
be given to him and explained. The writer is in the habit of 
devoting at least three or four lessons (of about an hour each)- 
to this all-important part of the subject. As mentioned above, 
it is of the utmost importance that the pupil should not only 
understand but prove to himself (by repeating before his teacher)* 
the existence or absence of “ voice" in each letter therein 


contained, for this is the key to his difficulty, and he must be 
able to point out at onoe the first “ voiced ” letter in any word 
from him. With a view to fixing the recollection of the voiced 
and voiceless letters respectively in the pupil’s memory, Prof. 
Wyllie has drawn up a set of sentences for the use of stammerers, 
reproducing the consonants in groups according as they are 
voiced or not. These sentences by his kind permission are here 

A. Initials that contain voice. (In the pronunciation of these 
the voice is to be thrown boldly into the initial.) 

1 . “ Even ancient elves are awed over oozing.” 

2 . “ We visit the Zulus like ramblers yearly.” 

3. “ Best gold dust.” 

4. “ My nephew.” 

B. Initials that do not contain voice. (These are to be touched 
off lightly, the voice being brought out promptly in the ensuing 
vowel or voiced consonant.) 

1. “ Far shores seem thinly hazy.” 

2 . “ Two poor comrades.” 

It is often advisable to give additional sentences for practice 
upon the specially difficult letters in each pupil’s case, and until 
the patient has got quite familiar with the distinctive method of 
dealing with voiceless and voiced consonants respectively, it is 
well to restrict the sentences to the one class of consonants, so 
that he may not be confused by the change required suddenly to 
produce the others correctly. Thus to give a few illustrations :— 

A. Voiced — 

“ Davy Doldrum dreamt he drove a dragon.” 

" Gaffer Gilpin got a goose and gander.” 

“ Mother make more mustard; no, no, not now.” 

B. Voiceless — 

“ Five fat friars fanning fainting flies.” 

“ Two teetotums totally tired trying to trot to Tadbury.” 

“ Peter Piper picked a peck of pepper.” 

The pupil can, of course, easily draw up seutences containing 
the specially difficult initials for his own practice daily, and when 
he is familiar with the proper treatment of each class of con¬ 
sonants, each sentence should contain voiceless and voiced 
initial consonants, so that he may acquire the habit of promptly 
touching off the former and emphasising the latter. I have 



found it often very helpful in gaining the patient’s confidence in 
my ability to help him—a matter of no little moment in the 
treatment of a neurosis—to show to him even at the first lesson 
how such a common word, e.g. as “ Yes ” (which very often causes 
difficulty) can be readily enunciated by him by the emphasising 
of the vocal element in the initial. The pupil thus gets an 
insight into the practical side of the treatment, which will 
encourage him in the process—to him at first sight rather 
elementary—of learning anew the alphabet again. 

Special attention should be paid, of course (as given above 
with full details), to the method of dealing with the more 
troublesome letters L, R, J, etc., the management of W and Y, 
and particularly the proper enunciation of words commencing 
with “ wh,” as illustrated in such a sentence as—“ When will 
you walk yonder?” which he is to pronounce thus—“hoo-en 
oo-ill ee-ou 00 -alk ee-onder ? ” It is often useful to note the 
words which cause the patient most difficulty in reading or talk¬ 
ing, and get him to practise these by forming them into sentences 
to be repeated at his subsequent lessons. 

In all his lessons—his practising at home as well as those 
in presence of his teacher—the patient should stand up and 
speak out in a full (not necessarily loud) voice, and he should 
also follow Wyllie’s suggestion of “ making music with the voice, 
and listening to it as he speaks,” i.e. cultivate the habit of 
attending specially to his vocalisation. 

Undoubtedly another extremely important point to attend to 
is the cultivation of the habit of keeping always an ample supply 
of air in the chest to enable the patient to fully vocalise each 
appropriate letter. The tendency to speak—or attempt to speak 
—from a relatively “ empty chest ” is very common amongst 
stammerers, largely, no doubt, because so much of their breath 
is fruitlessly wasted in trying to produce orally letters which 
should originate in the larynx. In some cases, however, there is 
also deficiency in the expansion of the lungs from faulty methods 
of respiration, so that in such instances there is not merely a 
waste of air but a deficient store of it to begin with. Exercises, 
therefore, to improve the capacity of the chest as well as the 
control of the exit of air from the lungs will be found advan¬ 
tageous in most cases. It is scarcely necessary to mention that 
the pupil should constantly endeavour to avoid speaking abruptly 


or hurriedly, cultivating instead a deliberate (but not monotonous) 

Each of the pupil’s daily lessons should commence with the 
reading of Wyllie’s stammerer’s sentences given above, followed 
by careful practising of additional sentences (drawn up at first 
by his teacher, later by himself) containing exercises upon the 
consonants which especially cause him difficulty, and particularly 
any words which prove stumbling-blocks to him in his daily 
conversation (as noted by his teacher or himself). The next 
stage is to advance him to the reading aloud—perhaps enunci¬ 
ating is the better descriptive term—of poetry; the simpler 
forms, such as Scott’s, do admirably, especially some of the songs, 
e.g. in “ Lady of the Lake,” to take just a couplet in illustration 
of the way in which the writer tries to emphasise the vocal 
element in the voiced words, while the voiceless initials are 
“ filed down ” (as it were) to the smallest possible size. Thus— 

“ He is gone on the mountain, 

He is lost to the forest,” 

is to be enunciated as if spelt phonetically— 

“ He is (u)gone on the (om)mountain, 

He is (ul)loet^'oo the forest.” 

Note how the terminal “ t ” of “ lost ” is made to act as initial 
for the vocalised fragment of the succeeding word as explained 
previously. It is not long before the pupil learns the art of look¬ 
ing ahead, as it were, for the voiced letters upon which his energies 
are to be chiefly expended, and if the lines are spoken slowly and 
impressively it is quite possible to emphasise the vocal elements 
without exaggerating them. Blank verse may later be tried, and 
last of all prose as reading exercises. 

When the pupil is going over his lessons with his teacher, 
any stumbling or error of enunciation should, of course, be noted 
by the latter and the proper method of producing the difficult 
consonant explained. In this connection it may be mentioned 
that in nearly every case it will be found that the pupil is much 
worse at certain times than at others ; if he shows signs of being 
worse than usual at his lesson—stumbling at words which for¬ 
merly caused him little trouble—it is usually advisable to dis¬ 
continue the lesson promptly, for his unsatisfactory efforts will 
only make matters worse owing to nervousness. It may perhaps 



be not amiss to indicate the time ordinarily devoted to the pupil 
by the writer in treating cases. Usually I get him to come on 
successive days (for about an hour) till the whole of Wyllie’s 
alphabet, etc., has been explained—say fire or six lessons in all. 
Then he is asked to return twice weekly for a fortnight to re¬ 
peat his lessons and allow of observation on his carrying out the 
instructions given. Thereafter a monthly practice for about 
half an hour before his teacher for six months or so is usually 
sufficient to keep him on the right lines towards recovery, pro¬ 
vided the pupil is earnest in his desire to be cured, and persistent 
in his home practisings of about half an hour daily. 

This last point is the real crux of the whole matter. Some 
stammerers are indifferent to their lot; often, no doubt, as the 
result of fruitless attempts at so-called “ cures ” ; these pupils it 
will be very difficult to cure, for patient persistence in practising 
is the essential above all others in overcoming their difficulty. 
It should be remembered that it is not only the learning of the 
correct method of enunciation which is required, but in many 
cases there is also the unlearning of the faulty method (which 
comes so naturally from long usage), and this is even more diffi¬ 
cult, or at least calls for more watchfulness on the pupil’s part. 
On the other hand, a pupil who is eager to master his difficulty, 
and willing, therefore, to think before he enunciates (and not let 
the words come out anyhow), and practise vnth persistence on the 
lines laid down for him, will find not merely marked improve¬ 
ment result therefrom as the weeks pass into months, but at an 
increasing rate as his sense of being able to conquer his former 
difficulties thereby lessens his previous nervousness. The cure 
of such a deep-rooted (though functional) affection is by no 
means easy, but the chief difficulty is not in getting the pupil 
to understand the treatment, but in getting him to carry this 
out perseveringly. 

No definite rule can be laid down with regard to the age at 
which treatment should be begun. While it may not be easy to 
get young pupils to understand exactly the physiological principle 
upon which Wyllie’s treatment is based, his simile of the violin- 
player to illustrate the mechanism of speaking can be understood 
by children ; the really important question is the pupil’s earnest¬ 
ness in desiring to master his difficulty, and his willingness to 
persist in his lessons—a matter more of personal characteristics 


than of age in most patients. While it will be gathered from 
the above remarks that the prognosis in each case depends 
mainly on the will-power and determination to practise of the 
particular pupil, the writer does not by any means share in the 
serious views of some who would almost look upon stammering 
as an affection tending to shorten life from the strain upon the 
nervous system. Like many other functional conditions it may 
prove somewhat intractable, but surely it is very rarely fatal. 

At the outset I stated that Wyllie’s method of treatment of 
stammering was of such a nature as rendered it equally suitable 
for the general practitioner and the specialist; in the somewhat 
lengthy account given of it above I trust that description has 
not been belied. What is called for, however, I venture to think, 
is a wider recognition by teachers of medicine of the fact that 
stammering is not merely a condition within the purview of our 
profession, but a neurosis which any practitioner ought to be 
competent to treat upon scientific lines, instruction in which 
should form a part of his undergraduate clinical and systematic 

In conclusion, the subject of prophylaxis calls for a brief 
notice, viz. the question whether a pupil who stammers badly 
should be educated along with other boys, as in a public school. 
There is no doubt that in several instances stammering is largely 
acquired by a process of imitation, so that in this view the 
stammerer is a source of danger to others ; while, as regards his 
own comfort and happiness, the presence of a crowd of school¬ 
mates—not by any means always sympathetic—is too often a 
source of aggravation of his neurosis. There is, moreover, the 
further practical point, that in much of the class teaching prompt 
and hurried answering by the pupils is necessarily called for, the 
very conditions which will increase the stammerer’s nervousness 
and impediment If the pupil is trying to carry out at home 
(under the supervision of his medical attendant) the physiological 
methods described above for overcoming his neurosis, the good 
effects of this will be largely neutralised by the hurried (often 
competitive) viva voce work at school under conditions which 
make it well-nigh impossible for him to follow out properly the 
correct methods of utterance. In some cases, therefore, especially 
where the pupil is unusually sensitive and shy, or the impedi¬ 
ment is exceptionally severe, it will probably be better for the 


pupil (and his class-mates) that he should be taken from school 
and placed under the care of a tutor, who, in addition to carrying 
on his general education, can supervise the physiological treat¬ 
ment of his stammering under the instructions of the medical 
adviser upon the above lines. 


By Dr 0. CROUZON, 

Chef de Clinique k la Faculty de Medicine de Paris (Clinique 
M4dicale de l’Hdtel-Dieu : Professor Dieulafoy). 

On the 21st of January 1907, there was brought to the Hdtel- 
Dieu, bed No. 20, in the salle Saint-Christophe, a man of forty 
years of age, an accountant by profession, who had lost all power 
of walking. Some minutes before he had been walking on the 
Boulevard St Michel, when he was suddenly seized with weakness 
in the legs, which caused him to fall in a heap. He was brought 
to hospital, and at the present time it is still impossible for him 
to move the lower limbs. 

On uncovering the patient and examining his legs, we are 
immediately struck with the diminution in their size, with the 
muscular atrophy of the limbs from the knee; this is a kind of 
citrophie en jarreture which affects specially the gemellus, 
peroneal, and antero-extemal muscles of the leg, and the tibialis 
anticus muscle in particular. This atrophy is not limited to the 
muscles; it affects the bones also, and palpation of the tibiae 
shows that their dimensions are smaller than normal. Moreover, 
the tibia of the right side presents a callus, which corresponds to 
a cutaneous cicatrix. The callus and the cicatrix are both the 
results of a compound fracture which he had sustained thirteen 
years before from the fall of a heavy weight on his leg. The 
feet are deviated and deformed; they turn inwards; the great 
toe bends inside the middle line and tends to approach the 
posterior part of the foot. The anterior portion of the foot 
droops, and in walking the patient leans upon this anterior part, 
and upon the outside edge of his foot. The sole is hollowed out 
into a well-curved arch, and this plantar arch has to be sustained 


in walking by orthopedic shoes. The deformity is what is known 
as equi no-varus club-foot. Attempts have already been made to 
straighten the foot, for when patient was ten years old, section 
of both Achilles tendons was performed. The scars of this 
operation are still visible. 

Examination of the tendon reflexes does not reveal any 
disturbance of the patellar reflexes, which are almost as marked 
as normally ; but the Achilles reflexes are diminished. Diminu¬ 
tion of the reflexes would thus appear to be limited to the areas 
of muscular atrophy. There is no foot-clonus. Examination of 
the plantar reflex causes no movement of the toes; there is no 
Babinski sign. 

Sensibility is absolutely intact. There are no sphincter 
troubles. The trophic or vaso-motor troubles are very slight; 
they consist merely in transitory perspirations, or in sensations 
of cold in the feet. 

The patient has always been aware of these deformities of 
his feet; he says that they date from his infancy, that in the 
first months of his life he suffered from convulsions, then from 
paralysis. His convalescence was slow, and for a long time he 
had to walk with some orthopedic apparatus, which was at first 
applied to the whole of his lower limbs and the waist, then to 
the legs and thighs, then to the legs alone, and finally, when he 
was about fourteen, he could come and go without the aid of any 

The case was evidently one of an infantile atrophic paralysis. 
The site of the paralysis, the integrity of the reflexes, and the 
absence of any spasmodic phenomena lead us to the diagnosis of 
infantile spinal paralysis. 

The objective signs of this paralysis, and the evolution which 
we have just recorded, do not in themselves present any interest¬ 
ing peculiarity. 

On the other hand, the history of the patient from the age 
of fourteen seems worthy of note. Contrary to what is observed 
in most cases of infantile paralysis, where the disease once 
terminated leaves only some infirmity without any morbid 
return, we have here a series of paralytic accidents in the 
lower limbs which have re-appeared during the last twenty-two 

At the age of 18 (the patient could walk without any 



0. CR0UZ0N 

artificial support since the age of 4), he found one day, on trying 
to rise from the table, that his legs would not carry him; he 
was put to bed and for four months his lower limbs were para¬ 
lysed. He does not seem to have had any fever. The paralysis 
did not extend to other muscular territories, and the atrophy of 
the muscles affected in childhood was not aggravated. After 
this period of four months, patient felt some tingling in his legs, 
and gradually began to walk again. 

At the age of 22 (four years later) one evening on returning 
from the theatre, he fell on the Boulevard Sebastopol; he was 
put into a conveyance and taken home: there he was put to bed, 
where he remained for three months in the same condition as on 
the former occasion. Again he commenced to walk. At the 
age of 25, on coming from his work, he fell in the Avenue de 
l’Opdra; he was taken home, and lay paralysed in bed for two 
or three months. 

At the age of 29, whilst walking one day on the Boulevard 
St Michel, his legs gave way under him: he was taken to the 
Hdtel Dieu, salle St Denis, and there he remained for six weeks, 

At the age of 35 he was in Rouen; he felt unwell one 
evening, went to bed, and had fever. Next morning, on trying 
to rise, he fell on the floor. He was put back to bed, and the 
fever continued and lasted for three weeks: he had, he says, 
mucous fever. 

During the convalescence from this fever, he attempted to 
rise; but all movement of the lower limbs was impossible. 
He remained paraplegic for eight months, and then gradually 
regained power of walking. 

At the age of 39, in October 1906—that is, three months 
ago—he fell on the Place Maubert and was taken to the 
H6pital de la Piti^, into M. R^non’s ward, and there he remained 
three weeks. 

In November 1906, some weeks later, he again fell down 
in the Boulevard St Germain; again he was taken to La Piti4, 
where he remained fifteen days. 

Finally, quite recently, at the commencement of the month 
of January, he fell down in the Rue de Rennes; he was taken 
to La Charity, into M. Toupet’s ward, where he remained until 
some days ago. When he left hospital, he was walking almost 


quite well; but again his legs gave way on the 21st of January, 
which necessitated his being brought to the H6tel Dieu. 

From the age of 18 to that of 40, that is to say, in the space 
of twenty-two years, this patient who had been the subject of 
an old spinal paralysis, has thus been affected by nine returns 
of attacks of paraplegia, which have been transient, and not 
accompanied by fever, and which have been neither accompanied 
nor followed by any progress of the paralysis. 

The case is, without doubt, one of spinal accidents resulting 
from the infantile paralysis. 

These tardy spinal accidents of acute anterior poliomyelitis 
are now well known. There is no longer any question of 
regarding this affection as a simple infirmity without any ulterior 
effect, related to a definite cicatrix of an inflammatory focus 
in the cord. We must refrain from concluding with Ross, 
“ that subjects who have been affected by infantile paralysis 
do not really seem more exposed during the course of their 
existence to other affections of the cord, than those till then 
free from any internal lesion.” 

Indeed, this writer’s views have been contradicted by the 
observations and works of numerous authors. Raymond pub¬ 
lished in 1875 the first observation of progressive muscular 
atrophy following infantile paralysis. Then came the works of 
Hayem, Quinquaud, Coudoin, Seeligmuller, Oulmont and Neumann, 
Sanze, Landouzy, and Ddjerine. 

The paper by Ballet and Dutil, and the thesis of Sattler, have 
brought the question to a point, and have established a definite 
classification of these spinal accidents. 

We might mention also the later publications of Grandou 
and of Bernheim, the clinique which Brissaud has devoted to 
late muscular atrophies following infantile paralysis, and finally 
the work of Pierre Marie on late scoliosis in infantile paralysis. 

Taking into consideration all the facts to which we have 
alluded, we may, with Ballet and Dutil, classify the late spinal 
accidents after infantile paralysis in the following way:— 

(a) Congestive attacks, with paresis or transient paralysis. 

(5) Acute myelitis in the form of acute adult spinal 

(c) Sub-acute myelitis in the form of sub-acute anterior 
spinal general paralysis. 


0. CR0UZ0N 

. (d) Chronic myelitis in the form of progressive muscular 
atrophy. The statement of this classification at once make* 
it evident that our observation belongs to the type of “con¬ 
gestive attacks with paresis or transient paralysis.” 

Leaving aside, then, those spinal accidents which assume ther 
type of acute spinal paralysis of the adult, of sub-acute generalised 
anterior spinal paralysis, and of progressive muscular atrophy^ 
we shall confine ourselves to some considerations with regard 
to the first type of paresis or transient paralysis superposed upon 
an old infantile paralysis. , 

This type is described by Ballet and Dutil in the following 
terms : “ An individual bearing the indelible stigmata of an old 
infantile paralysis, having, for example, one slender and atrophied 
lower limb, but experiencing on account of this infirmity merely 
a more or less marked awkwardness in walking, which renders 
it difficult and less secure, but does not completely impede it, 
is suddenly affected, without apparent cause, or under the in¬ 
fluence of cold, by complete or incomplete paralysis of the lower 
limbs. This paralysis is transient, and disappears after some 
hours or some days, but may not impossibly return later.” 

These writers quote in support of their description a personal 
observation, certain details of which are characteristic : it is the 
history of a man of 34 years of age, who was affected in the early 
years of his infancy by a paralysis of the lower limbs. His limbs 
were atrophied and showed vaso-motor troubles. In spite of 
this paralysis he could take somewhat long walks, and during 
the siege of Paris and the Commune he figured amongst the 
combatants. But in 1871 (patient was then 22 years of age, 
and was a prisoner at Versailles on account of the affairs of the 
Commune), he found one morning that he could not raise himself 
out of bed. He remained in this condition for a whole day. 
Already, in the preceding winter, on coming out of his office, 
he had suddenly experienced great difficulty in standing. From 
that time until the age of 25, this weakness of the legs became 
so marked every winter as to render walking exceedingly diffi¬ 
cult. In order to get along, patient was then obliged to lean 
upon a chair, which he pushed in front of him. When spring¬ 
time came, the strength partly returned to his lower limbs. 

In this case we have evidently a syndrome analogous to that 
presented by our patient. But our case appears to be still more 


characteristic, as the patient has had nine attacks of paraplegia. 
Moreover, in his case the attacks of paraplegia lasted several 
weeks or several months, whilst Ballet and Dutil allude merely 
to paraplegia of some hours' or of some days’ duration. The 
anatomical basis of these attacks of paraplegia has never been 
ascertained, and it is only by analogy with certain medullary 
congestive phenomena, such as the oedema and congestion of 
transient Pott’s paraplegia, that we can relate those transient 
paralytic troubles to a congestive process taking place in the 
circumference, or in the neighbourhood of the old cicatricial 

But whatever may be the value of this interpretation, the 
clinical fact none the less remains, and it will be of service to 
recognise it, in order that we may be able to look forward to the 
satisfactory evolution of a paraplegia occurring suddenly in an 
infantile paraplegic. 

• Still, though the prognosis is not grave, and though, the 
paralytic troubles may easily and rapidly disappear, it is none 
the less true that after a certain number of returns of paraplegia 
the weakness of the lower limbs may become persistent In 
our case it became gradually established, and in the intervals 
between the attacks the patient no longer recovered unimpaired 
his power of walking. The patient of Ballet and Dutil, three 
years after his attack of paraplegia, was seized one morning on 
rising by a complete paralysis of the lower limbs, which still 
persisted eight years later, with the addition of atrophy and 
progressive enfeeblement of the muscles of the lower limbs. 

So, then, we may agree with Sattler that successive inflam¬ 
mations, by diminishing the vital resistance of a cord already 
not uninjured, will by so much increase its morbid receptivity. 
It prepares the way for other more serious local affections, which 
will find, in the enfeeblement of the patient, a condition exceed¬ 
ingly favourable for their evolution. 


• Ballet and Dutil. Rev. de mdd., 1884 ; Gaz. Medicate, janvier 7, 1887. 

Bernheim. Rev. de mdd., 1893. 

Briasaud. “ Livre sur lea maladies nerveuses ” : Deuxieme e6rie. 

Carrieu. Thkse de Montpellier, 1876. 

Coudoin. These de Paris, 1879. 

Grand on. Thise de Paris, 1894. 


Hayem. Bulls, de la Soc. de Biologic, 1879. 

Quinquand. Bulls, de la Soc. de Biologic, 1879. 

Laudouzy and Dejerine. Rev. de mdd., 1888, Nos. 8 and 12. 

Pierre Marie. Soc. de Biol., October 1900, voir Lezden Festschrift, 1902. 
Onlmont and Neumann. Oaz. mdd. des Paris, 1881. 

Raymond. Soc. de Biologic, Avril 24, 1875. 

Roes. “ Diseases of the Nervous System,” tome ii. 

Sattler. Thise de Paris, 1888. 

Sauze. Thise de Paris, 1881. 

Seeligmuller. Jahrbiicher f. Kinderheil., t. xiiL, p. 315. 

Vulpian. Clinique mdd. de la Charitd, 1879. 




(134) (Recherches cytologiques sur le ddveloppement de la cellule 
nerveuse.) Rkmt Collin, Le Nevraxe, Vol. viii., Jan. 1907, 
p. 185. 

This elaborate memoir (extending to 123 pages) proves of 
particular interest to the writer, as it has appeared almost 
contemporaneously with a paper by him, dealing extensively with 
the same theme. It is remarkable to find how closely the main 
results of these two papers correspond. Collin’s observations are 
founded almost entirely on an examination of chick-embryos. 

One of the most important observations is the high degree of 
metabolic activity which he finds manifested by the nuclei of the 
neuroblasts. This activity is shown by a pronounced disturbance 
of the nuclear chromatin, a fact which the writer has also recorded 
in the chick. Collin describes two kinds of nucleoli in the neuro¬ 
blast-nucleus—chromatic and plasmatic. The chromatic nucleolus 
tends to divide into two smaller bodies, this phenomenon being 
frequently accompanied by a corresponding invagination of the 
nuclear membrane, which reminds one of an attempt at amitosia. 
The plasmatic nucleolus is not present in the neuroblast-nucleus 
from the first. Its date of appearance is variable, and this begins 
in the form of a small acidophile particle which gradually enlarge* 
The author has been unable to decide definitely upon the real 
significance of this body. 

Collin also describes the presence of a large number of fine 
granules in the nucleus during the early stages. He calls these 
chromatic microcaryosomes. The chromatic nucleoli are more or 



less spherical during the early stages, but tend later to break up 
into spherules which scatter throughout the nucleus. These 
spherules group themselves into grotesque patterns, some of which 
remiud one of the phenomena of karyokinesis. The various kinds 
of particles which are met with in the neuroblast-nucleus may be 
divided into those which are basophile and those which are acid- 
opbile. Collin finds that the basophile material is discharged 
from the nucleus to form the Nissl bodies, while that which is 
acidophile in nature, always retains its position within the nucleus. 
This observation is confirmatory of Scott’s recent work on this 

A large amount of evidence has recently been brought forward 
by Held, Rohde, Holmgren, Scott and the writer to show that the 
material constituting the Nissl bodies is, in part at least, a deri¬ 
vative from the cell-nucleus. This may be termed the nuclear 
theory of the genesis of these structures, in contradistinction to 
the usually accepted cytoplasmic theory. The results of Collin’s 
researches go to support the nuclear theory, for he describes the 
shedding of the basophile nuclear material into the cytoplasm in 
the form of the above granules to form the Nissl bodies. This is 
somewhat similar to the results of Rohde and Holmgren, but 
rather different from those of Scott and the writer, who hold that 
the nuclear derivative is not discharged as solid particles, but in 
the form of a fluid substance. The writer finds that the latter is 
achromatic in nature, afterwards becoming rechromatised outside 
the nucleus to form the Nissl bodies. 

Collin studied the neurofibrillary network, chiefly by means 
of the Cajal silver method, which in his hands appears to have 
yielded very satisfactory results. In this way he has been in a 
position to controvert Bethe’s statement that the long peripheral 
fibrils of the dendrons are distinct from the general network in 
the body of the cell. Collin describes the two systems of fibrils 
as blending freely with one another. The endocellular neuro¬ 
fibrillary network is developed before the Nissl bodies, according 
to Collin. He suggests a possible nuclear origin for this network, 
but as yet is not definitely decided on this point. 

Fragnito, Capobianco, Pighini, and other Italian neurologists 
have described in the chick, and also in other vertebrate types, 
the occurrence of a fusion of the nuclei of what they term the 
secondary neuroblasts to form the cytoplasm of the future nerve 
cell. Collin, like the writer, has been unable to satisfy himself 
of the existence of this phenomenon. If one makes a series of 
transverse sections of the spinal cord of the chick at any stage 
(say the tenth day), and stains these with aniline dyes, such as 
toluidine blue, methylene blue, or thionine, then the nuclei appear 
to have an indistinct contour, which suggests a process of fusing 



of these elements. If, however, another series of sections from 
the same specimen be stained by iron-alum-haematoxylin (as em¬ 
ployed by both Collin and the writer), then the various nuclei 
will be found to possess a sharp outline, thus preserving their 
individuality. The latter stain is undoubtedly the best to employ 
for studying the nuclei of the neuroblasts. 

Collin dismisses as untenable the theory which Kronthal has 
lately brought forward, regarding the development of nerve cells 
from the fusion of leucocytes. Very few embryologists will feel 
inclined to tender their support to Kronthal’s idea of nerve cell 

The numerous figures illustrating Collin’s paper have been very 
well executed. An extensive bibliography is appended. On the 
whole, the contents of this memoir will be found to constitute a 
distinct advance in our knowledge of the ontogeny of the nerve 
cell. John Camkbon. 

(135) (La Terminaison centrals des Nerfs sensibles p&iphdriquea. 

Le Nerf OochMaire.) Van Gbhuchten, Le Nevraxe , Jan. 

1907, p. 127. 

Very little work has been devoted to determining accurately the 
central termination of the cochlear nerve. Only Thomas, Weigner, 
Wyrubow and Tricomi-Allegra have used Marchi’s method for this 
purpose, and they all found degeneration in tracts which have 
been generally regarded as belonging to the secoudary acoustic 
system, i.e. in the corpus trapezoides, striae medullares, the superior- 
olives and the paraolivary nuclei. Van Gehuchten, who will not 
accept their conclusions, argues that degeneration is found here 
only because on intracranial section of the eighth nerve the brain 
stem is also invariably damaged, and partly owing to the fact that 
when the facial nerve is injured so intensely that acute retrograde 
degeneration occurs in its central end evidence of degeneration is 
always found in the corpus trapezoides and the other structures 
through which the nerve passes on its intra- medullary course. 

His own investigations consisted of the isolated destruction of 
the cochlear ganglion in the internal ear in guinea-pigs and the 
examination of the brain-stem after a suitable interval of time by 
Marchi’s method. In this way he was able to obtain degeneration 
of all the fibres of the cochlear root without injury to any other 
structure. He found that all these root fibres terminate in the 
tuberculum acusticum and the ventral nucleus, and that none of 
the root fibres extend into the corpus trapezoides, the striae medul¬ 
lares, or reach the superior olives. Gordon Holmes. 




(136) OPTIO BUNDLE. (Le faisceau longitudinal infdrieur et le 
faisceau optique central.) Lasallk Archambault, Nouv. 
Icon, dt la Salpiiribre , Nov.-Dee. 1906, p. 561. 

In a previous paper (reviewed in this Journal, Vol. iv. p. 31) the 
author recorded the results of his investigations, according to 
which the anterior end of the so-called inferior longitudinal 
bundle, or better the external sagittal layer of the temporo-occipital 
lobe, consists of a certain number of association fibres, plus the 
•central optic tract or the geniculo-calcarine fibres, which represent 
the cerebral path of visual impulses; while its posterior portion 
in the occipital lobe contains practically only geniculo-calcarine 

These conclusions were attacked by the Dejeriues, and the 
present paper is a reply to their criticisms. He first points out 
that his conclusions have been misinterpreted by his critics, and 
secondly, he argues that cases which have been published by the 
Ddjerines are confirmatory of his views. He insists that in every 
case in which a lesion destroys the primary optic centres or the 
retrolenticular segment of the internal capsule, secondary degene¬ 
ration is found in the occipital lobe only in the external sagittal 
layer, in which consequently the corticopetal fibres must be 
contained; they terminate along the lips of the calcarine fissure. 
Another point of interest is that, according to the author, the 
connection between the occipital cortex and the external geniculate 
"body is chiefly by corticopetal fibres (geniculo-calcarine, i.e. the 
true optic radations), while that of the occipital cortex with the 
pulvinar is almost entirely by corticofugal fibres (thalamic 
radations). Gordon Holmes. 


(137) Priorltftt in Sachen der Kontinuit&tslehre des Oentralnerven- 
systems.) B. Haller, Neurolog. Central hi, 1907, p. 118. 

Until the introduction of Golgi’s impregnation method, the 
•doctrine of continuity of the nerve elements had been accepted 
by most investigators. Golgi, on the strength of his silver pre¬ 
parations, proclaimed the central nerve-network to be a myth, 
though later, in 1894, he was less dogmatic on the subject. “ The 
misleading results of the Golgi method,” says Haller, “ were largely 
<lue to the ignoring of other staining methods.” As a consequence, 
the Neurone theory sprang into existence, and, for a time, dominated 
the field of neurology. Kolliker, the chief supporter of the Neurone 
theory, maintained the doctrine of neurones anatomically inde- 



pendent, in contact with each other but not in continuity. Now 
the swing of the pendulum is reversed, and many of the former 
most vociferous supporters of the Neurone theory have become 
its destructive critics, notably Nisei. Haller complains that the 
credit of the theory of continuity of nerve elements belongs to 
himself, and not, as Pfliiger has stated, to Apdthy. In conclusion, 
Haller gives a list of his own writings to prove his claim to 
priority. Purves Stewart. 



premieres Manifestations de la Fonction nerveuse dans la Vie 
embryonnaire des Vert6br6s.) Giacomo Piohini, Le Nevraxe, 
Vol. viii., Jan. 1907, p. 177. 

The results which are embodied in this brief note are founded on, 
a study of the movements executed by developing embryos of 
Pristiurus, Scyllmm, Mustelvs and Torpedo , which were kept under 
observation by the author at the Zoological Station, Naples. 

Pighini finds that the first spontaneous movements are observ¬ 
able when the embryo is about 25 mm. long. These become very 
free when the embryo has attained a length of 30 mm. At the 
stage when these movements are first exhibited Pighini finds that 
the central nervous system of these animals consists of a compli¬ 
cated network formed by chains of neuroblasts, while at the same 
period the multicellular character of the peripheral nerves is also 
very evident. The embryonic nervous system of selachians at 
these stages of development thus presents the type of nerve- 
network met with in the coelenterata and echinodermata. The 
author points out that the nervous functions exhibited at these 
early stages may be considered as the expression of the activity of 
a nervous system, which has not yet attained to the type of struc¬ 
ture met with in adult vertebrates. The contents of this all too 
brief paper afford strong support to the multicellular theory of 
development of the neuron. John Cameron. 


portamento di alcuni fenomeni riflessi dopo la sezione delle 
radid posteriori.) Ottorino Rossi, Rivist. di Pat. nerv. e merit., 
Jan. 1907, Vol. xii., p. 1. 

After exposure of the cord in the dorsal region, stimulation of 
a posterior root excites generalised reflex movements with groau- 
ng of the animal. If now one root be cut—in an animal that 



is not anaesthetised—and the peripheral nerve be stimulated, 
similar movements occur not only in the muscles corresponding 
to the nerve but over the whole body and the animal groans 
just as before. 

The author links these facts to Sherrington’s familiar experi¬ 
ments which shewed the great difficulty of obtaining anaesthesia 
by the section of any one root. He surmises that the stimulus 
overflowed to the other nerves still supplying the skin concerned. 
This is confirmed by the fact that section of two roots above, 
and two below the nerve experimented on, prevents the above 
phenomenon, the movements being then confined to the local 
group of muscles. 

The importance of being aware of the above occurrence 
is pointed out, as many contradictory experiences are thus 
avoided. Ernest Jones. 


MATHEMATICAL PRODIGIES. Frank D. Mitchell, Am. Journ. 

(140) of Psychol ., Jan. 1907, p. 61. 

In a somewhat lengthy paper the author gives a summary of the 
chief particulars known regarding twenty-four mathematical 
prodigies (of whom only one is a woman) described in literature; 
an account of his own case; and some conclusions regarding 
mental calculation based upon the foregoing data. 

His data do not enable him to speak of the influence of 
heredity. Precocity in calculation he finds to be normal. Skill 
in mental calculation is independent not only of general education, 
but of mathematical ability and education. Although mental 
arithmetic develops naturally out of counting , the fundamental 
operation is multiplication. Various mathematical and psycho¬ 
logical short-cvts explain the speed attained by some of the 
prodigies in their mental operations. The distinction often made 
between memory and calculation is misleading; the process is 
always a true calculation. Many of the calculators hitherto 
supposed to belong to the visual memory type turn out to be of 
the auditory (or auditory motor) type, at least in calculation. At 
least two of the major prodigies, however, and possibly four, 
belong to the visual type. A convenient table facilitates 
comparison of the different cases described. 

W. B. Drummond. 


(141) EPILEPSY. John Turner, Journ. of Meat. Sci., Jan. 1907. 

This is an elaborate investigation into the microscopical anatomy 
of the brains of persons dying from epilepsy. Upon his observa- 



tions the author bases his view that epilepsy is a disease occurring 
in persons with a defect of the nervous system, either congenital 
or involutional, and in whom also there is an abnormal state of the 
blood, characterised by a special tendency to intravascular clotting, 
and that the fits owe their exciting cause to sudden stasis of the 
blood stream, resulting from blocking of the cerebral vessels by 
these clots in some portion of the cortex. 

(a) The evidence of intravascular thrombosis, which is the 
novel feature in the pathology of epilepsy advanced by the author, 
is found in the presence of large numbers of blood-plates forming 
clusters within the cortical vessels. When appropriately stained, 
they are found to be rich in phosphorus, a fact indicating their 
nucleo-proteid nature. These bodies often amalgamate, so as to 
form cylindrical masses, entirely filling up the lumen of a capillary 
or bigger blood-vessel. The intra vitam formation of these clots 
is shown by the fact that proximal to them the blood-vessel 
is frequently distended and ruptured, giving rise to ecchymoses 
of red corpuscles. 

(b) Sclerosis and atrophy of small areas of the cerebral 
convolutions are frequently found, most commonly in the 
cornu ammonia, the cerebellum, and the parietal or occipital 
lobes. The author ascribes these atrophied areas to starvation 
and deprivation of their blood supply, arising from the thrombi 
which be finds so constantly present in the brains of epileptics. 

(c) Nerve Cells .—The cortical nerve cells in epileptics show 
two types of change, the one congenital, the other degenerative. 
The former should be regarded as ** stigmata,” as they are found 
more especially in persons of under average intelligence, the 
changes being very, clearly seen in the Betz cells of imbeciles. 
The latter, or degenerative changes, are similar to those induced 
by experimental ligature of the cerebral blood-vessels, and the 
author ascribes the condition to the interference with the cortical 
circulation arising from intravascular clotting. These changes 
consist of swelling of the nucleus, degeneration and death of the 
cell, aud eventually its complete disappearance. 

The author claims to have shown that among his cases 70 
per cent, showed defective structure, and 90 per cent, showed, in 
the form of thrombi, a blood Btate capable of acting as an exciter 
of convulsions. The impaction of thrombi accounts also for the 
patchy degeneration of the nerve cells, as well as for the isolated 
areas of sclerosis and atrophy so common in the epileptic brain. 

In an interesting addendum to the paper the author gives 
some observations upon the coagulability of the blood in epileptics. 
He found the difficulties considerable and the results by no means 
conclusive, but he formed the general opinion that, in most cases, 
there was, at or about the time of fits, a distinct acceleration of 



coagulation. The mean coagulation time in 28 epileptics on 135 
occasions was 120 seconds; in 13 cases of insanity on 38 occasions 
it was 136 seconds. 

The bulk of the paper consists of a full and detailed account 
of the pathological appearances of the central nervous system of 
41 cases of epilepsy. Wm. Aldben Turner. 

(142) OF THE BRAIN. (Hypertrophic, Hyperplasia, und Pseudo- 
hypertrophie des Gehirns.) Marburg, Arbeit a. d. near61. Inst it. 
a. d. Wien. Univ., Bd. 13, 1906, S. 288. 

This paper is a contribution to the question of diffuse glioma of 
the brain, which sometimes leads to a considerable increase in its 
weight and size. In this condition the chief characteristic is a 
hyperplasia of the neuroglia, diffuse or circumscribed, with which, 
however, may be associated a true hypertrophy of the nerve cells 
and nerve fibres. To those cases in which softenings or other 
destructive processes of the nervous tissues have occurred, with a 
secondary overgrowth of the neuroglia, the author has applied the 
term “ pseudo-hypertrophy.” 

True hypertrophy may be found unaccompanied by a hyper¬ 
plasia, but this is very rare. It is not associated with any clinical 
symptoms, and frequently the intellectual development of the in¬ 
dividual is good. Cases of marked hyperplasia, however, are 
usually met with in epileptic idiots. 

The hyperplasia may be diffuse or circumscribed. In the 
former case numerous axis-cylinders and fibres are still preserved 
throughout the affected region, but in the latter condition they 
are met with only near the periphery. 

With regard to the causes of these conditions, some authorities 
suggest that the hyperplasias may depend on the innate capacity 
of glia cells to proliferate; but the author considers that they are 
due to an embryonal or early infantile inflammatory process. 

But when the hyperplasias are combined with a true hyper¬ 
trophy of the nerve cells and fibres, the condition must have a 
different origin. 

It is impossible to imagine that an increase of the hemispheres, 
it may be up to three times the normal, can take place in the 
adult. They must therefore be congenital, although a neoplasm, 
in the form of a circumscribed glioma, may develop later. 

Some authorities have suggested that they may spring from a 
wandering germ cell which has retained its embryonal characters. 
This origin might explain the circumscribed tumours, but it could 
hardly be applied to the diffuse growths. 



The author then discussed at some length the relations ex¬ 
isting between growth of tissues and the secretions of the ductless 
glands. The influence of these may be indirect, e.g. through the 
disturbances of the blood circulation, as in the case of the supra¬ 
renal bodies, or direct, as in the case of the thyroid. 

He referred to several cases which have been described by 
other observers in which brain hypertrophy, hyperplasia, or other 
mal-formations have been present in cases which showed some 
alterations in the thyroid, thymus, hypophysis, epiphysis, or 
suprarenal bodies. Generally too, in these cases, more than one 
of these glands were affected. But whether the hypertrophy and 
hyperplasia are to be attributed to a deficiency or excess of 
secretion is not known. R G. Rows. 

(143) POSTERIOR SPINAL ROOTS. (Studien nr normalen 
and pathologischen Anatomic der hinteren Riickenmarks- 
wurzeln.) Levi, Arbeiten a. d. neurcl. Instil, a. d. Wien. Uni- 
versitdt, Bd. 13, 1906. 

The author’s research is confined to that part of the posterior root 
where it joins the cord. In all segments there is a glial layer 
which envelopes the roots and sends processes in between the 
fibres, forming a thick network on joining the connective tissue. 
This junction of the glial and connective tissue elements of the 
root is found in the cervical region, situated inside the cord, and in 
the lumbar and sacral region outside; but in the dorsal region it 
takes place at the cord margin. The diminution in calibre which 
takes place where the root pierces the pia arachnoid coincides only 
in the dorsal region with the above-mentioned point. 

Where Schwann’s sheath is lost and the glia begins, one finds 
that apparently the medullary sheath is wanting too, giving rise 
to the clear ring seen by the Weigert method. This clear ring 
indicates where the peripheral nerve becomes part of the central 
nervous system, and in the dorsal and even in the cervical region 
may correspond in situation to that point where the root undergoes 
a constriction in passing through the pia This, however, is not 
the case in the lumbar and sacral cord. 

The changes in early Tabes are seen to commence where the 
medullary sheath loses its staining reaction, i.e. in the lumbar 
and sacral cord outside the constriction, so that this loses its 
alleged significance in the pathology of the disease. 

David Ore. 




(144) INFANTS. (Uber Gewebever&ndenmgen im Gehim luetischer 
Neugeborener.) Ranks, Neurol. Centralbl., Nos. 3 and 4, 

Fifty brains were examined at varying periods of development, 
ranging from the third month of foetal life to some months after 

The author found proliferative changes in the capillaries, and 
in the intima of the arteries and veins, some of the latter being 
filled with endothelial cells. In ‘ % many instances plasma cells 
infiltrated the adventitia; and although passing beyond the limits 
of the lymph sheath, the infiltration was restricted to the tissues 
around the vessel. The neuroglia showed proliferative changes. 
In addition to diffuse lesions there were isolated foci, in which 
were recognisable plasma and mast-cells, elongated adventitial 
elements, and neuroglia hypertrophy. When these were present 
in the cortex, they were associated with nerve cell degeneration. 
In three cases spongioblasts were found. 

The pia was opaque and infiltrated by plasma cells, fibroblasts, 
and large round cells. 

The above pathological changes are the result of persistence 
of normal proliferation, in consequence of syphilitic irritation. 

In two cases the author found spirochoetae in large numbers 
amougst the endothelial cells of the vessels, in the muscular coat, 
in the adventitia, and even in the brain substance. 

David Orr. 


(145) IN PUERPERAL ECLAMPSIA. (Die Befonde am Zentral- 

nervensystem bei der puerperalen Eklampsie.) Po t t, a if 

Arbeiten a. d. neurol. Instil, a. d. Wien. UniversUat, Bd. 13, 

In the ten cases investigated, the anterior cornual cells, the 
nuclei of motor cranial nerves, the cells of Clarke’s column, and 
those of the spinal ganglia all showed more or less severe changes 
affecting both chromophile elements and the nucleus. The gang¬ 
lion cells of the posterior horns showed much less alteration than 
those of the motor cells. The glia cells also showed alterations. 

In the cerebral cortex the large pyramidal cells were affected, 
the chromophile material being collected at the cell base, and in 
many there was evidence of phagocytic action. 

The degenerative changes in the cord did not show a like inten¬ 
sity in all areas, but specially affected the motor cells. 

David Orr. 



cherches sur les changements des nearoflbrillee cons6cnti& &ax 
differents troubles de nutrition.) Marinbsco, he Nevraxe, Vol. 
viii., Fasc. 2-3. 

The author refers to the work of Cajal and Tello, who found that 
the neurofibrils undergo a considerable hypertrophy in animals 
exposed to cold, and who have suggested that this was a morpho¬ 
logical change due to the cold. This hypertrophy was also seen 
by them in cases of hydrophobia, and was attributed to altered 

Marinesco considers that they all result from disturbances of 

Changes in the chromophile substance often advance parallel to 
the affection of the neurofibrils; but sometimes the chromophile sub¬ 
stance may be considerably altered, while the neurofibrils remain 
intact. This is well seen in the hibernating hedgehog, in which, 
although the chromophile elements have largely disappeared, the 
neurofibrils are arranged regularly and are not enlarged. 

The author, as an explanation of this difference in results, 
suggests that it may be due to the fact that Cajal and Tello ex¬ 
amined the cells of cold-blooded animals, while he employed 
warm-blooded animals, in which a more active nutrition goes on 
during hibernation. 

In his experiments he has found that hypertrophy and coal¬ 
escence of the fibrils does occur in young dogs and cats if they 
are exposed to a temperature of 10°-15°, but exposure to tempera¬ 
tures below or above this (2* or 30°) leaves them almost intact. 
It is to be noted also that if a marmot, which falls into a hibernat¬ 
ing sleep at 6°, is exposed to a temperature of 0 # , it awakens, and 
begins to shiver and produce heat. It is possible that the tume¬ 
faction of the fibrils at low temperatures may be a means of 
defence against a dissipation of energy. 

It is not, however, a necessary result of low temperatures, or 
rather, it only occurs under special conditions. 

Further experiments have proved that hypertrophy and coales¬ 
cence of the neurofibrils are produced by various other disturbances 
of nutrition, and especially by intoxications, e.g. hydrophobia, 
morphia, strychnine, and moreover, a combination of these poisons 
with inanition or exposure to cold produces a much more marked 
alteration. R G. Rows. 



NERVE DEGENERATION. (La nature in time du processus de 

(147) Ddgdndrescence des Nerfs.) 6. Marinesco, La Pretse mSdicale r 
Feb. 16, 1907, p. 105. 

After remarking that almost nothing is known of the intimate 
nature of nerve degeneration, Marinesco reviews briefly our 
knowledge of the morphological and chemical changes which 
occur in the process of Wallerian degeneration. He believes 
that both the axolysis and myeline changes are the result 
of a species of digestion by means of ferments secreted by 
the nuclei of Schwann’s sheath. He gives a general account of 
some nerve transplantation experiments in support of this view. 
When a piece of nerve was transplanted under the skin there 
were some irregularly oriented apotrophic cells (cells produced by 
proliferation of the cells of Schwann’s sheath, which have a guiding 
influence on nerve fibres of new formation) but no new fibre 
formation. As the result of Auto- and of Homo-transplantation 
there was always new fibre formation and appearance of 
apotrophic guiding cells. These cells are the essential feature of 
both degeneration and regeneration. In cases of Hetero-trans¬ 
plantation there was no real Wallerian degeneration, but rather a 
necrosis. No apotrophic cells were formed. The piece of trans¬ 
planted nerve apparently provokes the formation of antibodies 
which are cytotoxic to it—hence there are no apotrophic cells 
formed, and consequently no degeneration or regeneration is 
possible. J. H. Harvey Pirie. 



(148) Ingbert, Journ. of New. and Ment. Dw., Jan. 1907, p. 2. 

After dealing with the classification of muscular atrophies, this 
paper describes a fairly typical case of pseudo-hypertrophic paralysis 
in a lad who died of typhoid fever at the age of 20. 

The pathological examination of the spinal cord showed nothing 
abnormal except some chromatolysis of the nerve cells of the 
anterior horn, which the author attributes to the typhoid infection, 
and a diminution in the number of nerve cells in the cord below 
the iouTth lumbar segment. 

A careful investigation of the nerve roots shows that there is a 
relative diminution of the size of the motor as compared with the 
sensory roots. 

In the left fifth lumbar motor root only 5171 nerve fibres were 
counted as compared with 10,366 in a corresponding normal nerve 



root; on the other hand, the normal root contains 4800 nerve fibres 
per square m.m., whilst the abnormal contains 4040. It is there¬ 
fore evident that the root investigated has a smaller area, contains 
a smaller number of fibres, and has a smaller number of fibres 
per square mm., that is to say, there is a greater diminution of 
the number of small fibres of the roots as compared with the large 
fibres. The muscles showed the usual changes. 

The pathological findings add support to the conclusion of 
other investigators that pseudo-hypertrophic muscular atrophy is 
primarily a disease of the muscles, and that the changes in the 
spinal cord and in the spinal nerve roots are secondary. 

F. K Batten. 

(OHARCOT-MARIE TOOTH TYPE). William G. Spiller, 
Joum. of Nero, and Ment. Dis., Jan. 1907, p. 14. 

This paper gives a good description of a case of progressive 
neuritic muscular atrophy, and compares it with a case of muscular 
atrophy having many features of the above type, but differing 
in that the proximal muscles were affected and contraction 
occurred. The pathological examination of the spinal cord in the 
second case showed no change. 

The author starts with the statement that, when first described, 
primary neuritic muscular atrophy was considered to be so sharply 
defined from other types of muscular atrophy that confusion 
could not occur. After detailing the characteristic features of 
the type, he seems to lay special stress on the almost constant 
absence of all contractions of tendons, and would hesitate to accept 
many cases described as progressive neuritic muscular atrophy 
because contractions were present. On such grounds it would 
be possible to refuse to accept the case here described, because 
there was no evidence that the disease had affected other members 
of the family, or had been transmitted from a previous generation. 

The fact whether contraction of tendons occurs, depends 
upon the relative affection of the antagonistic muscles, and 
although in most cases of neuritic muscular atrophy no con¬ 
tractions occur, yet to exclude a case from the group because 
contraction is present seems to me irrational. 

The author then gives a most excellent digest of atypical 
cases of neuritic muscular atrophy, and shows that many cases 
exhibit features which bring them into close association with 
other recognised types of myopathy. 

The paper concludes with the description of a case in which 
Dr Spiller hesitated to make the diagnosis of neuritic muscular 



atrophy, because the upper arm, thigh, and trunk muscles were 
much atrophied. Contractions were also present in the lower 
extremities. Section of the cervical and lumbar cord showed 
no pathological change, but the muscles showed long-standing and 
pronounced degeneration, F. E. Batten. 

MYASTHENIA GRAVIS. C. Eugene Riggs, Joum. Amer. Med. As*., 

(150) Dec. 15, 1906, p. 1969. 

In each of the three cases here recorded ophthalmoplegia was 
present in addition to the general muscular weakness. All three 
patients were males and their ages were 37, 35, and 45 respectively. 
In the first there was no apparent cause, in the second the 
symptoms came on shortly after an attack of influenza, and in 
the third a period of great anxiety and overwork preceded the 
onset. They all exhibited ptosis and the nasal smile, and the 
myasthenic reaction—the rapid exhaustion of the affected muscles 
by faradic stimulation—was obtained in each case. In the first, 
the diplopia was followed by myasthenia in less than a week ; in 
the second, two months elapsed between the onset of the diplopia 
and the first appearance of myasthenic symptoms; in the third, 
transient symptoms preceded the real inception of the disease by 
four months. One of the patients died after a year’s illness, and 
another was practically in statu quo a year after discharge from 
hospital. The third had been lost sight of but had probably 
since died. In discussing the differential diagnosis, the writer 
emphasises the difficulty of distinguishing between myasthenia 
gravis and hysteria in the early stages. As regards the pathology, 
there is probably circulating in the blood a toxin—perhaps the 
product of an enlarged or modified thymus, or an abnormal 
lymphoid tissue infiltration throughout the body—affecting the 
lower motor neuron. Strychnine, gentle massage, and galvanism 
were found to be the most efficient agents in treatment. 

Henry J. Dunbar. 

C HILDBIR TH IN ADVANCED TABES. (Eine Geburt bei vorge- 

(151) schrittener Tabes dorsalis.) Zacharias, Muench. med. 

Wochenschr., Feb. 12, 1907. 

Complete details are given of a case in which a multipara aged 
43, who had suffered for nine years from tabes, was delivered pain¬ 
lessly of a child. The unusual points were that the abdominal 
muscles did not come into action till the last four pains, when the 
head was being extruded; that there was absolutely no suffering, 
and that a rupture of the uterus appeared to be imminent towards 
the end of the labour. 

300 ; 


The tabes was well advanced, the chief symptoms being: 
immobile pupils, complete loss of superficial and deep reflexes in 
arms and legs, lightning pains, anaesthesia on the legs, diminution 
of touch and temperature sense on legs and ulnar side of arms, 
inco-ordination, and interference with visceral functions. 

John D. Comrie. 


un caso di tremore essenziale simulants in parte il quadra 
della sclerosi multiple.) Iginio Bergamasco, Bivist. di Pat. 
•M/rv. e merit., Jan. 1907, p. 4. 

The patient was a man of 64. He was admitted on account of an 
aortic aneurism, which killed him a few days later. On examina¬ 
tion of the nervous system, three abnormal physical signs were 
detected:—(1) Marked intention tremor in both arms; it was 
absent at rest, and increased on reaching toward an object; the 
oscillations were wide and slow, and affected first the fingers, then 
hands. There was no tremor of the lips, tongue, head, legs, or 
trunk. (2) Nystagmus, which occurred readily apart from any 
forced movement of the eye. (3) Speech slow and scanning. 
The first symptom had been present for fifteen years, the other 
two had been noticed for only eighteen months. 

At the autopsy the central nervous system was perfectly 
normal, even on microscopic examination, except for diffuse 
arterial disease and a recent (week old) thrombotic softening, the 
size of a bean, in the left cerebellar hemisphere. 

The writer points out the difficulty in diagnosis, and discusses 
the various causes of similar tremors. There was no other case in 
the family. Ernest Jones. 



Boston Med. and Surg. Journ., Feb. 7, 1907. 

The paper gives in detail the symptoms presented by a woman, 
aged 24, who presented some unique features. The complaint 
began suddenly, with pains down the legs and in the back, which 
in the course of three months became extremely severe, and were 
accompanied by increasing weakness, resulting in almost complete 
paraplegia within this time. Up to this time, as she was pregnant, 
the symptoms were attributed to this condition; but later she 
developed headache, mental aberration, complete anaesthesia below 



tiie waist, paraplegia, and bladder trouble. Nearly four months 
after the onset of the symptoms, the patient gave birth to a 
healthy child without pain, and without the use of the abdominal 
muscles. The points of peculiarity in the labour were its painless 
character, the absence of any instinctive use of the abdominal 
muscles, and the firm contraction of the uterus after labour, so 
that no haemorrhage occurred. There were no subsequent ob¬ 
stetrical complications. The patient died six months after the 
onset of symptoms. Post-mortem there was found an extensive 
'tumour of the spinal cord, destroying the lumbar region and 
associated with internal hydrocephalus. The occurrence of optic 
neuritis—quite unusual in tumours? of the cord—is explained by 
the writer as due to the hydrocephalus induced by the wide spread 
of the tumour. John D. Com&ie. 

MENINGITIS IN MUMPS. (Contribution k l’ltude do la mlningite 
(154) ourlienne.) Feliciano, Thkse de Paris , 1907. 

Meningitis in mumps may occur in children or adults, but in the 
latter, almost exclusively in men and in association with orchitis, 
like that which develops in typhoid fever, scarlatina, and other 
infectious diseases, meningitis complicating mumps belongs to 
the serous variety. The symptoms to which Dupre gave the 
name of meningism, correspond in most cases, as cyto-diagnosis 
proves, to a real inflammation of the meninges. “Ever since 
lumbar puncture has entered into current practice, meningism has 
lost ground, and its place has been taken by serous meningitis ” 
(Hutinel). The brain lesions are usually ill-marked in serous 
meningitis, but small extravasations of blood may occur, and even 
softening of the brain substance, as is manifested clinically by 
hemiplegia and aphasia. 

Three forms of meningitis in mumps are described. The first 
is an incomplete one in which the symptoms are so slight that 
a clinical examination must be supplemented by lumbar puncture 
to establish the diagnosis. Headache, pyrexia, and a slow pulse 
may be the only symptoms. The second form is one with com¬ 
plete symptomatology, but favourable evolution. Headache, 
vomiting, stiffness of the neck, and Kemig’s sign are present. 
■Occasionally ocular paralysis and delirium may develop. In two 
.or three days the symptoms disappear. In very rare cases aphasia, 
hemiplegia, or agraphia with difficulty of speech and uncertainty 
of gait may arise and persist The third is a grave form. The 
onset is the same as in the second, but the disease runs a rapidly 
fatal course. 



The fluid obtained by lumbar puncture is usually clear. In 
most cases there is a pure lymphocytosis. 

The prognosis is favourable as a rule. In most cases the 
meningitis remains serous, and the symptoms disappear fairly 
rapidly. The possibility of hemiplegia and aphasia must be con¬ 
sidered, but such complications are very rare. 

Treatment consists in the employment of hot baths several 
times daily. Lumbar puncture will often afford temporary relief. 
Leeches behind the ears, wet-cupping of the Bpine, cold applica¬ 
tions to the head, and such drugs as calomel, potassium bromide, 
and chloral, may also be employed with advantage. 

J. D. Rolleston. 

Vorkommen des Meningococcus und des Micrococcus Oatar- 
rhalis im Nasenrachenranm und Desinfectionsversuche mit 
Pyocyanase bei diesen Infectionen.) Jehle, Wien . klin . 
Wochenschr., Jan. 3, 1907. 

The writer states that this substance has been used as a germicide 
in anthrax, cholera, diphtheria, and typhoid fever. It is supposed 
to contain a bacteriolytic enzyme, and was used by him both 
against culture of the bacteria in question and in cases of natural 
infection. The method of experimentation was to add drops of 
the pyocyanase to one cubic centimetre of cerebro-spinal fluid or 
of normal salt solution containing organisms. After the lapse of 
various periods of time, attempts were made to produce cultures 
of the bacteria, generally in vain. 

With regard to patients suffering from influenzal attacks and 
having micrococcus catarrhalis in the nasal secretion, he found 
that after one application no more organisms could be obtained 
from the nose when 48 hours had elapsed. With regard to 3S> 
cases of patients suffering from and contacts with epidemic 
meningitis in whose nasal cavity the meningococcus was discovered, 
two applications at most were required to effect the disappearance 
of the organism. 

On the other hand the writer states that pyocyanase had little 
or no effect upon the streptococci, staphylococci, pneumococci, 
bacillus coli, and Friedliinder’s bacillus, commonly found in the 
nose. John D. Comrie. 




BT LUMBAR PUNCTURE. Darling and Wilson, Brit. 
Med. Joum., Feb. 23, 1907. 

This paper records a fatal case of sporadic cerebro-spinal meningitis, 
with the bacteriological findings in the spinal fluid. 

The organism present was a gram-positive coccus, which 
assumed bacillary form on Conradi-Drigalski medium ; did not 
liquefy gelatine; clotted milk; produced no indol; produced no 
gas in sugar-containing media; and was feebly pathogenic for 
rabbits. The writers believe it to be identical with the micro¬ 
coccus rheumaticus. They make some general observations upon 
the assumption by other cocci of the bacillary form, and give a 
photo-micrograph of the present organism in this state. 

John D. Comrie. 


(157) MENINGITIS. (Cellules de l’exudat dans la m^ningite cerebro¬ 
spinal 6pid6mique.) Speroni, Presse mid., Feb. 6, 1907. 

The writer gives the result of his examination of the cells pre¬ 
sent in eleven acute cases of this disease examined post-mortem. 
He found both in these, and in other acute cases examined by lumbar 
puncture, chiefly polynuclear leucocytes, many of which contained 
2 to 30 diplococci, in smaller number lymphocytes and large mono- 
nucleated leucocytes, alwaye more or less red-blood corpuscles, 
and finally fibroblasts. In more chronic cases of three to eight 
months’ duration, the lymphocytes and large mononuclear cells 
predominated; the polynuclears were few in number. 

John D. Comrie. 


and Wolf, Jrnrn. Am. Med. Ass., Dec. 29, 1906. 

This is record of a case in which a coloured infant died with 
symptoms of meningitis. Both on lumbar puncture and after 
death, organisms showing the various characters of the B. Diph¬ 
theria) were isolated by culture. The child after death showed 
various tuberculous lesions also. The writers state that they 
have been able only to find one previous case in which this 
bacillus was obtained from the central nervous system. 

John D. Comrie. 



(159) traumatischer Sp&tapoplexie.) Hochheim, Mueneh. med. 

Wochenschr., Jan. 29, 1907. 

The writer records the case of a workman, aged 34, free from 
Bright's disease or heart-disease, with healthy arteries and no 
history of syphilis, who nine weeks after a severe fall upon the 
back of the head developed a left-sided hemiplegia. Immediately 
after the accident he had to be helped to his feet and complained 
of great pain, but was able to resume his work. After some weeks 
he became foigetful and indifferent at work, and at the end of 
nine weeks one day was completely confused. The next night he 
became completely stuperose, the left face, arm, and especially leg 
were paralysed, and the sphincters relaxed. Within seven months 
recovery of mental power, control of the sphincters, and partial 
return of the use of hand and leg were established. 

The writer gives references to similar cases, and mentions two 
theories accounting for the connection of trauma with the apoplexy : 
that of Bollinger, that the injury causes a softening and necrosis; 
and that of Langerhans, that the cerebral vessels are damaged and 
weakened. John D. Comrie. 

(160) menologie der cerebralen Hemiplegia.) Z. Bychowski, Nettroloj. 

Centralbl., 1907, p. 155. 

Bychowski describes the phenomenon which has already been in¬ 
dependently recorded by Grasset and Gaussel (Revue Neurologique , 
1905, p. 881). It consists in the fact that in organic hemiplegia, 
whilst the patient can raise either lower limb separately from the 
bed in the supine posture (the hemiplegic limb being less power¬ 
fully raised than the sound one), it is usually impossible for 
him to raise both lower limbs simultaneously. Moreover, if the 
hemiplegic limb be raised alone, and we then passively lift the 
sound limb, the hemiplegic limb at once falls down. But whereas 
the French observers ascribe the phenomenon to the inability to 
fix the pelvis by the muscles of the hemiplegic side, Bychowski’s 
explanation is much less clear. So far as can be gathered from 
a somewhat involved statement, he ascribes the difficulty of 
raising both lower limbs to the fact that each cerebral hemisphere 
is accustomed to the performance of alternate rather than of 
simultaneous movements of the lower limbs; hence when one 
hemisphere is paralysed, the other hemisphere in the process of 
compensation succeeds better with alternate movements than 
with simultaneous ones. Furves Stewart. 




C. Eugene Riggs, St Paul Med. Jown., Jan. 1907. 

In both cases the tumour was situated in the posterior part of the 
second left frontal convolution and the adjacent motor area, 
giving rise to headache, epilepsy, aphasia, optic neuritis, turning 
of the head and eyes to the opposite side, and mental impairment. 
.A. full account of each case is given, and then the author discusses 
felie question of palliative operation in cases of brain tumour with 
regard to which his conclusions are as follows: 1. Palliative 
■operations should always be done early and before optic atrophy 
hias occurred. 2. Pain may kill. Headache, therefore, may be of 
such intensity as to demand this procedure. 3. Cerebral decom¬ 
pression should be regarded as a definite, recognised means of 
■surgical endeavour in every inoperable case. 

Henry J. Dunbar. 

TION. Alfred Gordon (Philadelphia), New York Med. 
Joum., Feb. 16, 1907. 

The two cases brought forward by the author may be placed, he 
contends, in the category of cases of amaurotic family idiocy, owing 
to the following characteristics—blindness commencing very early 
in life, mental deficiency from infancy, optic atrophy, and the fact 
that the two patients (brother and sister) were the offspring of 
Russian Hebrews. 

Briefly stated, the two cases were as follows:— 

Case 1.—Male set. nine years. Walked at nine months, spoke 
at two yea re. 

When he was twelve months old the mother noticed he could 
not see well. He has always been very backward and childish. 

At the age of three years he began to grow very stout, and 
this stoutness has constantly increased, although he eats very 

Thyroid gland impalpable, reproductive organs infantile, 
reflexes normal, slight instability of head. 

Patches of absorption of choroidal pigment in both eyes, with 
partied atrophy of optic nerves. 

Six fingers on each hand, and six toes on each foot. 

Case 2. —Female, set. thirteen years. 

Began to talk and walk at age of three years, and at same time 



blindness was noticed by parents. Very backward, foolish, and 
apathetic. Extremely stout, and gradually becoming more so. 
Thyroid gland enlarged. Optic atrophy. 

These cases the author considers very suggestive in view of the 
possibility “that some profound anomalies in the structure and 
function of the ductless glands are the real cause of the diffuse 
anomalous condition of the cells of the nervous system.” Both 
the recorded cases showed changes in the thyroid gland; from the 
illustration of the boy, his general appearance is seen to be 
markedly cretinoid ; and rather than reflexion on the possible 
relation between thyroid secretion and amaurotic family idiocy, 
one is forced to consider the propriety of classing these cases- 
under that term. A. Dingwall-Fordyce. 


Cushing (of Baltimore), N. Y. Med. Joum., Jan. 19, 26, 
Feb. 2, 1907. 

The first patient sustained a meridional fracture of the skull 
by a crushing force applied laterally. Extradural haemorrhage 
followed from rupture of the meningeal artery, and the patient 
exhibited compression symptoms, without preceding symptoms of 
concussion. A somewhat misdirected operation was followed by 
motor aphasia, which eventually cleared up almost completely. 
About three years later a pulsating exophthalmus developed, which 
was affected little or none at all by ligation of the internal carotid. 

In the comments upon this case the author refers to the 
extreme importance of the examination of the fundus of the eye 
in the determination of acute intra-cranial tension. With practice 
slight grades of venous stasis and early oedema should be recog¬ 
nised in the disc. The side upon which the pressure is being 
exerted can be readily determined by this means. In spite of the 
critical injury and its subsequent complications, the patient made 
good progress, and remained free from the most common sequelae 
of cranial injuries, i.e. “ post-traumatic neuroses.” 

The second patient was the victim of a penetrating stab wound 
of the skull. The left side of the braiu was punctured directly 
behind the middle of the Rolandic fissure; subcortical, post- 
central haemorrhage followed with contra-lateral sensory dis¬ 
turbances and visual word - blindness. An operation for the 
evacuation of the clot was followed by a rapid disappearance of 



all the symptoms except astereognosis. Faradisation of the motor 
cortex was performed. 

The author has been led to the opinion by this case and a 
series of others, that “a sufficient lesion of the hemisphere 
posterior to the sulcus centralis (Rolando), with no precentral lesion 
whatever, may produce motor symptoms which, however, are 
unaccompanied by degeneration of the pyramidal tract, and hence 
should not be regarded as a motor paralysis in the commou 
acceptance of the term.” 

The third case showed an old penetrating bullet wound of the 
skull, which involved the left frontal lobe. The patient suffered 
from epilepsy with vocal aura. An operation was followed by 
improvement, but not by recovery. 

In traumatic epilepsy of long standing, the author believes, 
that in the majority of cases the seizures are greatly lessened in 
intensity, and that in a small percentage they do not recur at 
all after operation. The gradual lessening in the severity and 
number of attacks is a more favourable sign than the immediate 
post-operative cessation. 

Concerning the psychic disturbances which follow a fracture 
of the skull. Bran has stated that in a study of 470 cases he found 
subsequent psychic disturbances in 34 per cent.; few of these, 
however, showed permanent alterations in mentality. English 
believes that some degree of mental impairment follows fracture 
in 10 per cent, of cases. Meyer estimates that these cases 
represent about 1 per cent, of asylum inmates. C. H. Holmes. 

(164) OF INFECTION. (Lea paralysies du moteur oculaire externe 
et la vote clphalorachidienne.) Fernand L&vy and Alphonse 
Baudouin, Rev. Neurol., Feb. 15, 1907, p. 102. 

The question of 6th nerve palsy following the introduction of a 
toxin into the cerebro-spinal canal is still quite recent. It was 
first observed by certain German surgeons following operations in 
which anaesthesia had been induced by the injection of stovaine 
into the lumbar part of the spinal canal. Two cases were reported 
in which diplopia followed this procedure; both recovered 
spontaneously, in the first case after six months, in the second at 
the end of a fortnight. In both cases about a fortnight elapsed 
after the operation before any signs of diplopia were noted. 
Boeder suggested, as an explanation, that the paralysis was due to 
the toxine of stovaine circulating along the subarachnoid space. 

The authors report two further cases following the deep in¬ 
jection of a mixture of alcohol and cocaine for trigeminal neuralgia. 



In the first case, that of a woman aged 50, two injections were 
made into the superior maxillary division, in the pterygo-maxillary 
fossa, without any ill effect. The inferior maxillary division was 
then injected at the foramen ovale. This was done twice, and 
immediately following the second injection a paralysis of the 6th 
nerve on the same side occurred. The condition still persisted 
at the end of a month, though it had improved somewhat The 
second case was similar in all respects to the first, but in addition 
to the 6th nerve palsy following the second injection, a slight 
degree of ptosis was noted also. On the eighth day the diplopia 
had disappeared. 

The authors discard any idea of the cocaine solution spreading 
into the orbit and causing paralysis in this manner, as the injection 
of the superior maxillary division was followed by no bad results. 
In their opinion some of the solution passed through the foramen 
lacerum medium and infected the subarachnoid space through 
which the 6th nerve passes, before entering the wall of the 
cavernous sinus. If this explanation is correct, the authors think 
that the paralysis is peripheral rather than central. The reason 
why the 6th nerve suffers in all these cases is not clear. It appears 
especially susceptible. The cases suggest the possibility of a similar 
path of infection in those transitory ocular palsies which are met 
with in acute and tubercular meningitis, as well as in secondary 
syphilis. C. M. Hinds Howell. 

Fisher, Ophthal. Rev., Feb. 1907, p. 31. 

Under this heading the author gives a full account of five cases 
which he has personally observed. He regards them as being 
probably allied to the cases recorded by Ormerod and Spicer in 
VoL xvL of the Transactions of the Ophthalmological Society , 
under the title of “ Recurrent Paralysis of Ocular Nerves.” The 
author does not think the term ophthalmoplegic migraine should 
be applied to these cases for two reasons: first, that the headache is 
not exactly of the type which is usually found in migraine; and 
secondly, because the term tends to detract from a search for an 
organic lesion, which has been discovered in some of the cases, and 
is, in the author’s opinion, probably present in them all. The 
pain is not necessarily unilateral, and the position of maximum 
intensity is variable—being occipital in two of the cases—retro- 
ocular, temporo-frontal, occipital and retro-ocular in the others. 

The opportunities for complete examination in such cases as 
the author describes have been few, but Giibler has described a 



plastic exudation in the basal subarachnoid space in one case, in 
which fibrous adhesions were also present around the origin of the 
third nerve. In other cases a fibroma or chondro-fibroma involving 
the ocular nerves has been described. No nuclear lesions have 
ever been noted. C. M. Hinds Howell. 

(Observation clinique et anatomo-pathologique des yeux d’une 
paralytiqne g4n4rale.) A Rodiet and Bricka (of Marseilles), 
L’Enciphdle, Sept.-Oct. 1906. 

The clinical examination of the patient, aged 35, showed sluggish 
reaction of both pupils to light; the left pupil was wider than the 
right, and showed only faint reaction to accommodation. Ophthal¬ 
moscopic examination showed a slight degree of optic atrophy. 
The histological examination disclosed an optic neuritis due to the 
proliferation of the connective tissue elements and the neuroglia 
between the bundles and nerve fibres of the optic nerve. The 
nerve cells in the retina showed inflammatory and destructive 
changes. The case is insufficiently reported. 

C. Macfie Campbell. 

PABALYTIO PTOSIS IN HYSTERIA (Le ptosis paralytiqne dans 

(167) Thystdrie.) Ch. Sauvineau, Rev. Neurol., Feb. 15,1907, p. 97. 

The author records two unusual examples of hysterical paralysis. 

The first case was that of a girl aged 11| whose mother gave 
the following history. The girl had been in her ordinary health, 
which was good, till a month previously. At this time she had an 
attack in church, felt sick, was pale, fainted for a short time, 
and afterwards slept for about an hour. 

Ten days previously awoke with complete bilateral ptosis. On 
examination the palpebral fissure on either side was reduced to 
about 3 mm. In order to see, the child held her head back* 
There was no overaction of frontales, or orbicularis to assist the 
paralysed levator palpebrse. There was no spasm of orbicularis. 
In addition, the child had a very well marked left hemiansesthesia, 
but without any limitation of the visual field. 

The diagnosis of hysteria was made, and a rapid cure effected 
by faradisation and suggestion. A relapse followed in a fortnight, 
but on this occasion suggestion alone sufficed to effect a cure, which 
has remained permanent. 

The second case was that of a girl aged 13. 



Two years previously she had suffered from phlectenular 
ulceration of the cornea, which had produced an intense photo¬ 
phobia—the condition relapsed from time to time. With the 
photophobia, blepharospasm developed, at first associated only 
with the presence of corneal ulceration, later becoming continuous. 
On examination the patient presents the following appearance:— 

On the left side there is a well marked condition of blepharo¬ 
spasm, which is accentuated when the child is told to open 
her eye, or when an attempt is made to do so. On the right side 
there is a partial condition of ptosis, unassociated with any 
spasm. There is marked overaction of the frontales, with elevation 
of the eyebrow. The head is carried thrown back, in order that 
the patient may see. 

There is no loss of sensation of any kind, and the child’s general 
health is excellent. The application of sparks from a high 
frequency apparatus was ordered, combined with statical electricity. 

As a result of this, during the first sitting, the ptosis cleared 
up, but the blepharospasm, on the other hand, made but slight im¬ 
provement, but gradually passed off during the next fortnight. The 
eyes were then examined for errors of refraction, and a compound 
hypermetropic astigmatism discovered. Glasses to correct this were 
ordered and so long as the child wears them, all goes well. If, 
however, they are removed, fibrillary tremors at once commence in 
both eyelids, at the same time the eyes oscillate quickly, the child 
never looking in any definite direction, or fixing any particular 

In conclusion, the author defines the diagnosis between ptosis 
and blepharospasm, laying special stress on the implication of the 
lower lid in the latter condition. He draws attention to errors of 
refraction as being a frequent source of tic and blepharospasm, and 
emphasizes the necessity of carefully testing for such errors, as 
they may otherwise escape attention. 

C. M. Hinds Howell. 


(168) (Uber Stdrungen im Bereiche des Hamapparates bei Hysteric.) 

Alfred Hock, Prag. Med. Woch., Feb. 7 and 14, 1907. S. 65 
u. 79. 

The author has shortly put together an account of the more common 
manifestations of hysteria that are seen in connection with the 
urinary apparatus. He emphasises the importance of their study 
and gives a series of instances in which serious operations had 
ignorantly been undertaken for their relief. 

1. He mentions first hysterical renal colic, which by its 



intense pain radiating along the ureter to the groin, severe 
strangury with suppression of urine, haematuria, vomiting, and 
pyrexia gives rise to the greatest difficulty in diagnosis; normal 
kidneys have frequently been incised and even removed through 
the error thus brought about. Two new cases are briefly described, 
one in a woman of 26, the other in a boy of 13. The occurrence 
of haematuria in hysteria has of course been much doubted, but 
recent exact observations have shewn that this symptom may 
undoubtedly occur. Hock mentions several other causes of 
haematuria proceeding from a healthy kidney. 

2. Hysterial nephralgia alone is usually attributed to mobile 
kidney, which explains the want of success that operations 
undertaken for this condition shew. 

3. The anomalies of urinary secretion in hysteria are two— 
excess and diminution. The polyuria is usually transient, taking 
place at the end of a hysterical attack ; only the watery constituent 
is increased. Permanent polyuria occurs chiefly in male hys¬ 
terics ; the commonest time is between the ages of 25 and 50; 
it may begin suddenly or gradually; the amount passed may 
exceed 40 or 50 pints a day; tenesmus is common in the con¬ 
dition, and retention, necessitating catheterisation, may occur; 
the chlorides are in excess, the other constituents not; in severe 
cases when the polydipsia does not equal the polyuria advanced 
wasting may ensue. 

4. Hysteric anuria is not so firmly established as a true 
undoubted phenomenon, in spite of Charcot’s teaching. Gilles 
de la Tourette distinguished between transitoi'y complete anuria 
and incomplete oliguria, and permanent anuria in which vicarious 
secretion takes place from the stomach, bowels, skin, and salivary 

5. The commonest bladder manifestation is cystalgia, usually 
diagnosed as irritable bladder. The urine is normal, but the 
mucous membrane is so sensitive that distension cannot be 
allowed and pollakuria is usually marked. Sphincter spasm 
may prevent the introduction of instruments. 

6. Hysteric retention is the best known symptom, though it is 
very rare. The author mentions a case in a man who had been 
catheterised daily for eighteen months. He was temporarily cured 
by suggestion but was admitted later into a strange hospital for 
retention, and ultimately died of an ascending infective condition. 
The author holds that the non-development of trabeculae in the 
bladder ( Balkeiiblase ) differentiates the state from retention due to 
organic nervous diseases, the commonest of which in this connec¬ 
tion is tabes. Hysteric retention is due in some cases to paralysis 
of the detrusor, with or without anaesthesia of the mucous mem¬ 
brane, in others to spasm of the sphincter. De la Tourette 



related a case of the latter variety in which the impassability of 
the sphincter led to the performance of urethrotomy. 

7. Hysteric incontinence is not so common, but marked cases 
are on record. The author records two, one in a woman of 23, the 
other in a woman of 20; in both cases there was complete anaes¬ 
thesia of mucous membrane, and ignorance as to the act of micturi¬ 
tion, until the skin was felt to be wet. In the former instance 
the origin of the condition dated to a New Year’s night when the 
patient—a servant—suddenly woke up to find her employer in 
her bed. To defend herself she passed water, and from that time 
had suffered from continual incontinence. Ernest Jones. 

(169) PERSONALITY. Morton Prince, Boston Med. and Swrg. 

Journ., Oct. 4 and 11, 1906, Vol. civ., pp. 372 and 407. 

In this paper, read before the Boston Society for Psychiatry and 
Neurology, Dr Prince discusses, from a purely clinical standpoint, 
the relation of hysteria to changes in the personality. Sometimes 
the physical manifestations of hysteria, the anaesthesias, paralyses, 
contraction of the visual field, etc., are the most prominent, and 
sometimes the mental, the moodiness, emotionability, aboulia, etc., 
but in both cases the essential mechanism—psychological disaggre¬ 
gation—is the same. The disaggregated portion may comprise a 
separate personality. It is well known that multiple personality 
is a type of hysteria. But the converse is not well recognised, 
namely, that hysteria is the disaggregation of the personality, so 
that the hysteric is a phase of multiple personality. 

Prince, in delineating multiple personality as a precise clinical 
group, has analysed twenty of the best reported cases. He points 
out that the notion of multiple personality has become strongly 
but incorrectly associated in our minds with the presence of 
amnesia, because our conception of the condition has been derived 
chiefly from those sensational cases in which there had developed 
an amnesia on the part of one of the personalities for the life of 
another. This amnesia is, of course, not a necessary phenomenon, 
and is seen only in pronounced cases. Every hysteric with 
changes in mood and character is potentially a case of multiple 

A typical mode of production of the condition is as follows. 
An ordinary hysteria develops in the usual way, gradually and 
without any loss of memory for the previous mental life; the 
patient slides, so to speak, into a condition exhibiting perhaps 
hemiansesthesia and contractures with changes in character such 
as moodiness, irritability, ugliness of disposition, etc. At such a 



time no suspicion would arise that we had anything other to deal 
with than classic hysteria. This condition may persist for many 
years, or even indefinitely, the patient remembering the whole of 
his previous mental life. Then, as a result of artificial interference, 
such as a hypnotising process, or after an emotional shock, the 
subject may suddenly become completely normal, unification of the 
personality having occurred. Again no suspicion of anything very 
unusual is aroused. But now it may be that a sudden and complete 
relapse to the previous hysteric state takes place; when this happens 
the hysteric will still remember his early life, but will have forgotten 
the whole of the experiences acquired while in the normal state. 
Amnesia is thus added for the first time. Frequently another 
phenomenon, that of alternation, may occur, so that we thus have 
a condition of multiple personality established. Prince points out 
two specially important facts; first, that the early abnormal state 
may show only mental symptoms and be diagnosed as pure neuras¬ 
thenia instead of hysteria, owing to the fact that finer dissociation, 
i.e. neurasthenia, frequently, or even usually, complicates hysteria ; 
and secondly, that if this early “neurasthenic” condition has 
persisted from childhood it may be thought to constitute the 
normal personality of a congenital psychasthenic, so that the 
synthetised normal state that supervenes, perhaps in middle life, 
may be wrongly interpreted as an “ abnormal ” secondary person¬ 
ality. This incorrect interpretation was until lately applied to 
several of the celebrated cases of multiple personality, including 
Felida X. and Marcelline R, and had aroused much speculation 
and astonishment at the greatly superior nature of this “abnormal” 
secondary personality. Ernest Jones. 

(170) der Hysterie bei Tieren.) H. Dexler, Neurol. Ceniralbi, Feb. 1, 
S. 98. 

This lengthy and somewhat diffuse article is mainly a critical 
appreciation of a recent publication of Mainzer’s. (See Review of 
Neurology , 1906, p. 513.) The author prefaces this by some theo¬ 
retic considerations of the mind of animals, particularly of dogs, 
as contrasted with that of man. He emphasises our ignorance of 
psycho-pathological processes in animals, which is due to the 
unhappy separation of neurological and veterinary studies. In 
general, he is rather opposed to the modern tendency to over¬ 
approximate the mental processes of animals and man and main¬ 
tains that the existence merely of language in the latter sets up 
an overwhelmingly important barrier. He illustrates his attitude 
by the following remarks. Epilepsy in animals is almost always a 
symptomatic secondary occurrence, the commonest cause being an 



encephalitis; the existence of this, by the way, can often be 
determined only microscopically. Gross lesions of the projection 
system in animals cause psychical symptoms much less frequently 
than in man, on account of the relative paucity of the association 
systems in the former. The structure of the brain in animals 
shows that the differences to be expected between them and men 
are not only quantitative, i.e. on a smaller scale, but also quali¬ 
tative. He admits, however, that more exact researches in 
comparative psychology have enabled one to detect more complex 
psychoses than was at one time thought. Just as word deafness 
in man has only of late years been distinguished from dementia, 
so in animals some of the insanities, with “object blindness,” etc., 
can be clearly distinguished from dementia. In dogs it is probable 
that intense disturbances of taste play at least as important a role 
as deafness in man; and affections of the sense organs are especi¬ 
ally difficult to define in animals, just as they are in idiots. Again, 
an outstanding difference between men and animals is the reduc¬ 
tion in the latter of the psychical symptoms compared with the 
somatic symptoms in such bodily diseases as cancer, severe infec¬ 
tions, etc. 

Coming now to the question of hysteria in animals the author 
holds that any affective complaint such as paranoia, typical 
hysteria, etc., is exceedingly rare if not altogether non-existent in 
animals. He has seen no such occurrence in the 6000 dogs he 
has observed for some time. Mainzer’s three cases of hysteria he 
considers of the greatest importance as no former cases had been 
observed with such detailed analysis by a neurologist of Mainzer’s 
standing. He thinks, however, that the diagnosis of hysteria is a 
little open to question, principally because of the difficulty in 
excluding other psychoneuroses, which are certainly commoner. 
He discusses the three cases in detail, and makes some interesting 
remarks on the symptom of agoraphobia in general, and of fear of 
certain localities in particular. He relates several interesting 
cases in which a definite memory symptom was present so that 
the animal—dog or horse—exhibited fear on coming to a spot 
where a previous painful episode had taken place. 

Ernest Jones. 

(171) du pied et signe de Babinski dans l’hystdrie.) A. Van 

Gehuchten, Le Ntvraxe, Jan. 25, 1907, p. 311. 

In a preliminary consideration of the reflexes the author calls 
attention to a syndrome, the importance of which he has empha¬ 
sised in previous communications, and to which he thinks other 
writers have not attached the importance which it deserves. It 



is a much exaggerated condition of the deep reflexes upon one 
side of the body in the absence of any sign of hemiplegia in cases 
in which a lesion of the opposite hemisphere is probable. He 
cites the case of a man who, after receiving a blow upon the left 
side of the head, developed local epilepsy, commencing in the right 
foot and spreading over the right side till the face was involved. 
He had no sign of hemiplegia, there was marked atrophy of all 
the muscles on the right half of the body. The right plantar 
reflex was of the extensor type. ** The tendon reflexes upon the 
right side were so exaggerated that the lightest percussion with 
the bent finger upon the tendon of any muscle produced a vigorous 
contraction of that muscle. 

He refers to his classification of the cutaneous reflexes which 
he published in Le Ntvraxe, Yol. i., 1900. This classification 
separates the superficial reflexes into two divisions. 

1. Abnormal or defensive cutaneous reflexes, perhaps patho¬ 

logical. These require for their production the integrity 
of the lower reflex arcs (spinal cord) only. They are the 
reflexes with which physiologists have worked, and they 
may be called the “ skin reflexes of medullary origin ” 
or the “ lower skin reflexes.” 

These are entirely and fundamentally distinct from:— 

2. The normal physiological or clinical cutaneous reflexes, 

which for their production require the integrity of the 
nervous system. 

These he terms the higher cutaneous reflexes. 

The author proceeds to argue at length against the somewhat 
bitter criticisms which Babinski has passed upon his classification 
and terminology. 

Van Gehuchten insists that, as the standard of every normal 
cutaneous reflex, shall be taken “ the minimal motor response to 
a minimal stimulus.” He insists that the normal or higher 
cutaneous reflexes are obtained only upon stimulation of a definite 
skin area, and that the response is always in the same muscle. For 
each of these reflexes there is a pre-existing centre in the spinal 
cord, with pre-determined afferent and efferent paths. 

For the abnormal or lower cutaneous reflexes there are no pre¬ 
existing spinal centres. Stimulation of the skin produces ever 
varying responses, now in one muscular region, now in another. 
He admits that the most constant and the most easily elicited re¬ 
action is Babinski’s extensor response, but he points out that the 
extensor response can usually be obtained by stimulating any 
part of the leg or thigh. He further emphasises the variability of 
this lower reflex by citing the fan response of Babinski, the 
abductor response of Hirschberg and Rose, Oppenheim’s reflex, 
Remak’s femoral response and the paradoxical response of Schaffer, 



and the flexor response produced on stimulating the skin of the 
abdomen, and many others. 

The detailed description of such phenomena is destitute of any 
practical value. The important fact which covers the whole 
ground is the variability of the abnormal or lower cutaneous 
reflexes as regards form and region, compared with the unvarying 
character of the normal or higher reflexes. 

This variability is a sign that the spinal cord is free from the 
influence of the higher centres, and that it has returned to the 
same physiological condition that obtains at a given moment of 
developmental life, and that is permanently present in the lower 
vertebrates—the spinal cord becomes a simple reflex mechanism 
destined for the defence of the individual against excitations which 
reach the cutaneous surface. 

Van Gehuchten then proceeds to the all-important question. 
Does the appearance of foot clonus, etc., and of the inferior 
cutaneous reflexes (Babinski’s sign, etc.), necessarily point to a 
lesion of the cortico-spinal fibres? May not these phenomena 
appear from functional derangements of the cortex, more par¬ 
ticularly hysteria ? He himself is inclined to a negative answer 
for the first question and a positive answer for the second. 

He cites the case of a young woman eighteen years of age who, 
after an attack of indigestion with vomiting, suffered with gradually 
on-coming weakness of the legs, foot clonus, and Babinski’s sign 
on both sides. There was partial hemianalgesia on the right 
side, the limbs and face escaping. A diagnosis of syringomyelia 
was made, but a good prognosis was given to the patient with the 
object of comforting her. Five days later all the signs had 
disappeared. It is interesting to read that Van Gehuchten had 
treated this patient three years previously for external strabismus 
which had recovered after treatment with arsenic. 

That such a distinguished neurologist as Van Gehuchten should 
have based this important opinion on this isolated case is unfor¬ 
tunate, for the antecedent ocular paralysis, in the reviewer’s opinion, 
stamps the subsequent transient spastic paraplegia as the early 
manifestation of disseminate sclerosis. 

Similar cases are by no means rare, and are generally recognised 
in this country since the publication of many contributions by 
Buzzard upon this very subject. 

The arguments, therefore, brought forward in this paper, that 
“increase of the deep reflexes and the appearance of the lower 
cutaneous reflexes with Babinski’s sign may be present in excep¬ 
tional cases of hysteria from psychic interruption of the cortico¬ 
spinal fibres,” leave the reader very far from being convinced. 

James Collier. 




(172) OF EPILEPSY. (Application de la diazo-r^action nrinaire an 
pronostic de l’6tat de mal dpileptiqne.) Paul Masoik, Joum. 
de Neurol ., Jan. 20, 1907, p. 21. 

This article is a repetition of several previous publications on the 
same subject. In spite of the many adverse criticisms that these 
have met with, the author hopes that their importance will in time 
be established. He first discusses the prognostic significance of 
hyperthermia in epileptic attacks, and agrees with the modern 
criticisms of BoumeviUe’s former views; the mortality in a series 
of cases was equal in attacks with and those without this 

He has studied the diazo reaction in detail in 16 cases, 
and has made the following observations. The reaction was 
positive in 6 out of 7 fatal attacks, and negative in 3 out of 9 
non-fatal attacks; in other words, 6 of the 9 positive cases died, 
and 1 of the 7 negative cases. From this he concludes that the 
presence of the reaction is a sinister indication, whereas its absence 
is of good import. The reaction may appear early, or at any time 
throughout; the earlier its appearance, the worse is the outlook. 

Other observations on the urine during the attacks shewed 
the frequent occurrence of albumin and acetone, but glycosuria 
was very rare. Ernest Jones. 


(173) (of Philadelphia), Joum. of the Am. Med. Ass., Feb. 9, 1907. 

The author discusses the relationship between alcoholism in the 
parent and the development of epilepsy in the child. From his 
own experience, he believes that the danger to the prospective 
child depends not so much upon the parents, one or both, being 
habitual drunkards, as upon their being intoxicated or under the 
influence of liquor at the time of conception. Echeverria, after 
the analysis of about 572 cases of epilepsy, concluded that 
parental intemperance established a predisposition to epilepsy in 
1730 per cent, of cases, while parental insanity associated with 
epilepsy antedated but 15‘96 per cent, of his cases. Molli finds 
that from 30 to 40 per cent, of all persons with drunken fathers 
are epileptics. Martin, after the examination of 150 insane 
epileptics, found that nearly 60 per cent, had intemperate parents. 
He also found that in 83 intemperate families with 410 children, 
108, or more than one-fourth, were epileptics. Bourneville states 
that from the examination of 2554 children suffering from idiocy, 
imbecility, epilepsy, and hysteria, he found that 1053 of them were 



the offspring of drunken parents, 983 had drunken fathers, and 80 
drunken mothers. Demaux reported 5 out 36 epileptics who were 
conceived when their fathers were intoxicated. Woods concludes his 
paper by citing two of his own cases: the first patient, while a tem¬ 
perate man, was the father of two healthy children; later, when he 
became intemperate, two other children were born, one of which 
developed epilepsy in his sixth year, while the other had paralytic 
dementia with epilepsy. In the second instance both the father 
and mother were moderately intemperate. Of eight children, 
three were epileptics. C. H. Holmes. 

NEUROSES AND PSYCHO - NEUROSES. (Ntooses et psycho- 

(174) n4vroses.) F. Raymond, L'Encdphale, Partie Neurolog., Jan. 

1907, p. 1. 

Professor Raymond proposes to publish a series of papers on this 
subject, with the intention, in view of its importance and difficulty, 
of making a critical exposition of the recent work done, and of 
defining his attitude towards some of the more disputed problems. 

In his preliminary memoir he gives us in a very general way 
his conceptions of the whole subject. He first insists on the cardinal 
importance of clinical truths, which are in the last resort the only 
definite ones, as they stand independent of all explanatory systems. 
He uses the term functional disease to signify a disease, not without 
a lesion, but without any known lesion. He clearly points out, 
however, that we are too ready to assume from this that a little 
more delicate research would demonstrate these lesions. It is 
very probable that they are not anatomical lesions in the gross 
sense in which we use this word, but chemical or physical; a 
magnetised bar of iron is indistinguishable from any other bar 
in every respect, except for one physical property. This point of 
view leads to a broader conception of the term organic lesion, 
a term which raises in our mind ideas of a visible deformity or 
destruction of certain nervous elements. 

Excluding the insanities on the one hand, and certain of the 
simpler neuroses, such as neuralgia, on the other, he limits himself 
to the grandes ndvroses, hysteria, epilepsy, hypochondria, psych- 
asthenia, etc. He restricts the term psychoneuroses to the border¬ 
land between the neuroses and the insanities {v6sanies\ in contra¬ 
distinction from the Germans, who include most of the latter in 
the term. The acceptance of the word indicates the new attitude 
that recognises the essentially psychic nature of the diseases, and 
was the forerunner of its natural consequence, psychotherapy. It 
is only within the past few years that such neuroses as hysteria 
and the tics have been recognised to be essentially mental diseases. 



As to the limits of the group of psychoneuroses, it is interesting 
to note that, until the appearance of Axenfeld’s volume in 1863, 
such conditions as tabes, hydrophobia, tetanus, etc., were included 
therein. Many diseases have been excluded since then, and 
Raymond now suggests that chorea, Parkinson’s disease, Grave ’3 
disease, and epilepsy be also excluded. In the last instance the 
group of symptomatic epilepsy has so encroached of late on that 
of idiopathic epilepsy as to threaten to involve it altogether. 
He would even exclude from this group of psychoneuroses, hypo¬ 
chondria and neurasthenia, thus leaving only two psychoneuroses, 
hysteria and psychasthenia. Hypochondria, he considered, should be 
counted amongst the vizantes. The question of neurasthenia is 
more difficult. Of late years its domain has so extended, includ¬ 
ing such diverse conditions as hypochondria, rudimentary paranoia, 
tics, all forms of ahoulia, etc., that Tanzi has appropriately named 
it the giant of neuropathology. “ Malheureusement, ce g&mt n’est 
pas seulement ddmesur^.il est informe.” Raymond considers that the 
neurasthenic state, comprising chiefly such symptoms as readiness 
to fatigue, insomnia, dyspepsia, headache, bad temper, irritability, 
etc., is only a syndrome that may be induced by numerous condi¬ 
tions, moral shock, infectious disease, organic nervous disease, etc. 
He would limit it to the neurosis described by Charcot as true 
neurasthenia, which is essentially an acquired one and curable. 

Iu opposition to this he supports Janet’s grouping of what 
Charcot termed congenital or constitutional neurasthenia, together 
with the obsessions, phobias, tics, scruples, aboulias, under the 
name psychasthenia. This is essentially a congenital condition, 
indications of its presence being manifested in childhood, and, 
though alleviable, rarely curable. 

Fortunately the practical question of treatment does not 
altogether depend on accurate grouping of the disease, because 
psychotherapy is fundamentally an individual treatment, varying 
more with the patient than with the disease. At the basis of all 
mental treatment comes the question of isolation. Separation 
from the family and old surroundings is invariably necessary, 
though the degree of isolation enforced varies from case to case. 
Raymond, however, agrees with all other modem authorities that 
the overfeeding and putting to bed employed in the Weir- 
Mitchell treatment is not the panacea it was formerly thought 
to be. Hydrotherapy, electrotherapy, and massage are discussed, 
and their limitations pointed out. Raymond does not think that 
hypnotism is free from serious inconveniences, so that it should 
not be employed as a routine measure; in exceptional cases, 
however, particularly in some forms of hysteria, it is necessary 
to have recourse to it, as one can in such cases achieve nothing 
without it. Ernest Jones. 



(175) HEADACHE AND MIGRAINE. (Disturbi psichici acuti 
transitori bu base ce&lalgica ed emlcranica.) M. A. Bioglio, 
JUvist. di Pat. nerv. e ment., Jan. 1907, Vol. xii., p. 9. 

The writer has studied these peculiar symptoms described some 
years ago by Mingazzini, and in addition the slighter disturbances 
that occur when the pain is less severe; he concludes that in 
both instances the nucleus of the disturbances is essentially the 
same. He first describes the following three cases:— 

1. Soldier, aged 24 After receiving a sharp remand he was 
seized with severe headache, which persisted, so that he had to lie 
down. He then became delirious, with visual hallucinations, and 
was transferred to an asylum. Cure was complete in two months. 

2. Widow, aged 39. She had suffered from chronic headache 
for many years, with migraine attacks at the menstrual periods. 
On the occasion of one severe attack she became delirious for 
eight hours, and had multiple visual hallucinations of a religious 
nature. This recurred and she was admitted to an asylum. 
During the intervals she was quite normal. 

3. Housewife, aged 37. Since the age of twenty she had suffered 
from attacks of lancinating and constricting fronto-occipital pains. 
During the nausea at the height of the attack she frequently 
experienced visual hallucinations of a simple nature—bright 
clouds, coloured fires, etc. These became more complex and 
organised after a psychical attack that followed the birth of her 
first child. 

4 Soldier, aged 21. He was a psychasthenic who had suffered 
from “ petit mal ” attacks since childhood. Of late years, especially 
after the ingestion of alcohol, he suffered from more complicated 
attacks, in which, after the appearance of violent frontal pain, he 
lapsed into a state of impulsive agitation—evidently a variety of 
automatism—and subsequently had profound amnesia for the whole 
of this period. These attacks were of a hysteric nature. 

The author points out the difference between the first group, 
cases 1 to 3, and the second, case 4. From a study of them, it is 
clear that acute psychical disturbances may be associated with 
severe pain in the head, both being due to a common cause, 
hysteria, epilepsy, etc., or—and this is the main point the author 
wishes to make—severe pain in the head may be the sole cause 
of marked psychical symptoms in an otherwise normal person. 

Ernest Jones. 



<176) BASEDOW’S DISEASE. (Contribution & l’dtude des troubles 
ment&nx de la maladie de Basedow.) C. Parhon and S. 
Marbb (of Bucharest), L'EncJphale, Sept.-Oct. 1906. 

The authors report two cases of Basedow’s disease with mental 
disorder. Both patients had a bad heredity; the first was a 
woman aged 35, the second aged 21. In the first case, the mental 
symptoms were mental instability, want of attention, irritability, 
erotic tendencies, hallucinations, ideas of persecution. The goitre 
had preceded the mental symptoms. In the second case, there 
were present terrifying hallucinations, distressing dreams, morbid 
anticipations, and great irascibility. The bilateral resection of the 
cervical sympathetic improved the physical condition of the second 
patient, but had no influence on the mental disorder. The authors 
review the literature on the association of exophthalmic goitre with 
mania, melancholia, paranoic conditions, conditions of hallucinatory 
confusion, and hysteria. They refer to two cases published by 
Boinet, where excessive doses of thyroid extract produced mental 
disorders such as have been observed in exophthalmic goitre. The 
authors are of opinion that, in the majority of cases, the mental 
disorders observed in this disease are due to thyroid intoxication, 
and are not merely casual associations. 

C. Macfie Campbell. 

(177) (Ein Fall von Dystrophia Musculorum progressiva hombiniert 
mit Morbus Basedow.) Liebers, Muern-h. med. Wochenschr., 
Feb. 19, 1907. 

Tue record is given with full details of the case of a woman aged 
23 in whom, since the age of 15, a progressive weakness and atrophy 
of the face, and of the shoulder-girdle muscles, with pseudo- 
hypertrophic condition of the deltoid, biceps and triceps, had been 
coining on. For some months, very distinct symptoms of Base¬ 
dow’s disease (trembling, rapid pulse, sweating, diarrhoea, anxiety, 
etc.) had come on. The writer regards the two diseases as being 
accidentally combined, and not causally related to one another; he 
mentions a similar case recorded by Moebius. 

John 1). Comuie. 



(178) (Die Schlaflosigkeit infolge von Sttirungen des Vorechlafes.) 

Karl Lechner (of Klansenburg, Hungary), Klinik f. psych, w. 
nerv. Kranhheiten, Bd. 11, H. 1, 1907. Carl Marhold, Halle 
a. S. 

The author in the present paper, which extends over twenty-three 
pages of this number of the Klinik, restricts himself to a pre¬ 
liminary analysis of the normal sleep reflex and a description, 
illustrated by clinical examples, of the principal forms of disorders 
of the first phase of sleep (Vorschlaf. Praedormitio). With 
regard to the analysis of sleep, Professor Lechner finds, besides the 
“ phylogenetically imparted and autogenetically accommodated 
periodicity,” only two incontestable criteria: unconsciousness and 
recuperation. These are two separate processes, generally but not 
invariably in direct relation to one another. A long sleep is often 
accompanied by deficient recuperation and vice versa. Also the 
depth of the unconsciousness does not always correspond to the 
resulting restoration, nor even in normal sleep do they run pari 
pasm. This is well represented by a chart which has been drawn as 
expressing the result of numerous experiments, sleep-depth having 
been calculated by the use of a specially constructed barsesthesio- 
meter and the degree of recuperation by Kraepelin’s method (the 
continued addition of single figures in definite periods of time). 
Professor Lechner gives two charts which show an abrupt increase 
in depth of sleep in the first, and an almost equally rapid decrease 
in the second hour, and later a more gradual wave-like progression 
to waking consciousness, whereas the restoration curve shows a 
uniformly undulating elevation; thus illustrating the separable 
nature of the two processes. The relations of these two events to 
vasomotor changes are next discussed, and the various forms of 
disturbances of sleep—described later—indicated, the whole of this 
part being summed up in the following:— 

1. That there are particular disorders of the praedormitio and 
others of the post-dormitio. 

2. That the disorders of sleep depth may be separated from 
those of the restoration. 

3. That according to their heterogeneous (external) or auto¬ 
genous (internal) origin, sleep disturbances are to be distinguished 
as exogenous or endogenous. 

4. That according to the results of sleep, that is, from the point 
of view of restoration, sleep disorders may be divided into hypos- 
thenic, hypersthenic, parasthenic, and palinsthenic forms. (By 
palinsthenic, Professor Lechner means all those in which a slight 
stimulus is followed by a great positive effect, and moreover, whose 
resultant does not correspond to the excitation in quality.) 



Professor Lechner then proceeds to a minutely detailed 
description of the quantitative and qualitative disturbances of the 
fore-sleep, the fundamental disturbances between sleep-depth and 
restoration being applied to the clinical categories. The whole 
paper is valuable and in many ways suggestive, but is unfortun¬ 
ately burdened with a novel and most cumbrous terminology. 


THE KNEE-JERK IN PNEUMONIA. Stanley Barnes, Birm. Med. 

(179) Rev., April 1906, p. 199. 

The author investigated the knee-jerk in sixty cases of pulmonary 
disease. In 48 the bacterial cause could be found. Four were 
empyemata due to various bacilli, in none of which the knee-jerks 
were affected. The remaining 44 were cases of pulmonary con¬ 
solidation. In 34 the pneumococcus was found, in 6 the tubercle 
bacillus, mixed septic organisms and bacteria of decomposition 
were present in 2, diphtheria bacilli and pneumococci together 
in one, and diphtheria bacilli alone in one case. The knee- 
jerks were diminished or abolished in all the cases of diphtheritic 
or pneumococcal pneumonia, unaffected in septic pneumonia, 
and unusually active in pulmonary tuberculosis. This condition 
of the knee-jerk is thus of diagnostic value in pulmonary disease. 
It has also some prognostic importance, early loss of the knee- 
jerk indicating profound intoxication. In Barnes’s cases loss of 
the knee-jerk always occurred some time before death if the 
bacterial cause was the pneumococcus. The date at which the 
knee-jerks disappeared varied from the first to the seventh day. 
Return usually occurred two or three days after the crisis. Ex¬ 
amination of the third lumbar segment in fatal cases showed that 
the only changes present were to be found in the large motor 
cells of the anterior horns which showed all the earlier stages of 
chromatolysis. J. D. Rolleston. 

MARIE’S VIEWS ON APHASIA. F. X. Dercum, New York Med. 
(180) Joum., Jan. 5, 1907, p. 7. 

The author refers to fourteen cases of aphasia and three cases of 
pseudo-bulbar paralysis which he has recently examined with the 
special purpose of testing Marie’s affirmations and conclusions. 
Applying (without criticism) Marie’s tests for intellectual impair¬ 
ment, Dr Dercum found in all the aphasic cases above referred to 
an unquestionable defect, “for all these patients were unable, 
although in varying degree, to comply with any but the simplest 



instructions.” Again he remarks, “Defective utterance of such 
words as were still preserved in the motor aphasics was common 
to all; though in some it was more pronounced, in others less 
pronounced.” In the only case in which anarthria was entirely 
absent, there was no impairment of motor speech. He concludes 
that Marie’s contention that aphasia is a unity, an anarthria added 
to an intellectual defect, is well borne out by the clinical facts. 
After discussing the question of Brocas convolution, he sums up 
by remarking that “ we are entitled to a legitimate doubt as to the 
real function of the left third frontal.” Edwin Bramwell. 

(181) phfoomdne de la ligne blanche, lliypotension arterielle et 
1’insufBsance surrdnale.) Sergent et Ribadeau Dumas, 
Bull. et. inim. de la Soc. mid. des Hop. de Paris, July 12, 1906, 
p. 757. Siredey et Tinel. Ibid., Feb. 14, 1907, p. 145. 
Massary et Ltan, Ibid., Feb. 21, 1907, p. 161. 

The phenomenon designated the “ white line ” by Sergent is the 
converse of the touche ciribrale, and is due to a spasm of the 
cutaneous capillaries. It was found by Sergent and Ribadeau 
Dumas in the various morbid conditions due to suprarenal in¬ 
sufficiency, viz., Addison’s disease, certain cases of neurasthenia, 
intoxications of different kinds, and acute infectious diseases, 
notably influenza, enteric, scarlatina, and diphtheria. In such 
conditions there is hypotension and peripheral vaso-dilatation. The 
mechanical stimulation of the skin produces vaso-constriction and 
the appearance of the “ white line.” The phenomenon is best 
produced by stroking the skin of the abdomen with a finger or 
other blunt object. Within thirty to sixty seconds a white streak 
appears, broader than the object which has produced it, and not 
surrounded by the pink zone characteristic of the white line which 
appears immediately on stroking the skin of a normal person. 
The white line persists from three to five minutes, and then 
disappears. The administration of adrenalin in some cases of 
diphtheria which presented the white line was followed by the 
disappearance of the phenomenon. 

In a case of tuberculous meningitis recorded by Siredey and 
Tinel in a man of 47 the appearance of the white line in place 
of the tache ciribrale suggested a lesion of the suprarenals. The 
blood-pressure was low, but there was no abnormal pigmentation 
of the skin or mucous membranes. The forecast proved correct, 
for the autopsy revealed not only tuberculous meningitis with 
pulmonary and peritoneal tuberculosis, but also large tubercles in 
the suprarenals. The liver and kidneys were not affected. 



Massary and Lian have recently reported two cases of insola¬ 
tion, in one of which they observed the white line, while in the other 
the tache c&rtbrale appeared. The two phenomena were regarded 
as due to the same cause, both being the result of meningeal 
irritation. The white line, according to Massary and Lian, is 
simply the result of a nervous disturbance, which may be slight 
and purely functional (physiological white line), but which in 
disease is due to a primary or secondary alteration of the nerve 
centres. This alteration is primary when the nervous system 
alone is involved, and secondary when the nervous system is 
affected by various morbid influences, among which must be 
included perturbation of the functions of the suprarenals. 

J. D. Rolleston. 


(182) AND PSYCHICAL DISEASES. (Ueber Art und Wert 
klinischer Oed&chtnismessungen bei nervosen und psychischen 
Erkrankungen.) Paul Ranschburg (Budapest), Klinik }. 
psych, u. nerv. Krankheiten, Bd. 11, H. 1, 1907. Carl Marhold, 
Halle a. S. 

SINCE the publication of his Stndien ueber die Merkfdhigkeit 
in the Monatsschr. f. Psych, u. Neurol, of 1901, reference has been 
frequently made by other workers who have used it to Dr 
Ranschburg’s “word-pairing” method. This consists essentially 
of presenting to the subject, either orally or exposed upon a screen, 
paired words, and then, after a definite interval, presenting the 
first word of each pair and testing the power of recall of the 
second. As elaborated by Dr Ranschburg, the method is of great 
importance both from the point of view of pedagogical inquiry and 
of psychiatry. The author limits the present paper to a general 
description of his method and its application to nervous and 
mental cases. Under definite and uniform conditions as to method, 
time, and length of exposure, character of verbal material, and 
duration of interval between the exposure and examination of the 
subjects, the memorial product can be expressed in terms approxi¬ 
mating to mathematical accuracy. The whole paper, which is 
not completed in this number of the Klinik , is so compact with 
information that it can hardly be described in less space than 
itself. R. Cunyngham Brown. 



ATTACKS IN DEMENTIA PILE COX. (Lea ictus dans la d6mence 

(183) prlcoce.) Pascal, L’Enctphale, Sept.-Oct. 1906. 

The author discusses the question of the occurrence of epileptiform 
and apoplectiform attacks in dementia prsecox, reviewing the 
opinions of previous authors. The occurrence of epileptiform 
convulsions raises the question of the relation of such cases of 
dementia prsecox to hysteria on the one hand, and to epilepsy on 
the other. Where the characteristic deterioration of dementia 
prsecox occurs in well-marked cases of hysteria or of epilepsy, 
with attacks dating far back, the author concludes that there is 
merely an association of the neurosis with dementia prsecox. But 
convulsive attacks may occur in cases of dementia prsecox which 
have shown no other evidence of hysteria or epilepsy, and where 
the attacks must be attributed to the basis of the psychosis itself. 
The relation of the attacks to the psychosis is variable. The 
attacks may precede the psychosis by a long period; they may 
first occur after the psychosis has been well established, or they 
may immediately precede the development of a rapid dementia. 
The attacks in dementia prsecox are usually convulsive in nature; 
apoplectiform attacks are rare. The difference between the 
attitudes of various authors is shown by the fact that the author 
diagnoses as dementia prsecox two cases with convulsive attacks, 
which Janet has reported as cases of hysteria and psychasthenia. 
As to the pathogenesis of these attacks, we know practically 
nothing. C. Macfie Campbell. 


(184) INSUFFICIENCY. (Confusion haUncinatoire aigue et 
insuffisance hlpatique.) G. Deny and M. Renaud (of La 
Salpetriere, Paris), L'Encephale, March-April 1906. 

The patient was a woman of 38, with no psychopathic disposition, 
neither syphilitic nor alcoholic, who after several years of gastric 
disorder, rather quickly developed a condition of hallucinatory 
confusion with vague ideas of persecution, fears of poisoning, and 
general apprehensiveness. The clinical examination of the viscera 
was negative, the bowels were irregular, the tongue diy and coated; 
patient quickly became feebler; diarrhoea developed, and there 
was evidence of intestinal haemorrhage. The autopsy disclosed 
an atrophic condition of the small intestine, with some small 
haemorrhagic areas; the kidneys showed diffuse parenchymatous 
alterations; the liver showed very marked general fatty degene¬ 
ration; the central nervous system showed well-marked cellular 
changes; there was no inflammatory element present. According 



to the author, the following is the interpretation of the case; the 
patient had a slight gastro-intestinal affection; the liver was 
uu.ible to exercise its normal rdle, and the mental disorder followed 
upon this hepatic insufficiency. The renal insufficiency accen¬ 
tuated the auto-intoxication. Clinically, the mental disorder was 
almost the only expression of the hepatic insufficiency. 

C. Macfie Campbell. 

(185) (Beitrag zur Psychologic der Aussage. Auf Grand eiues 
gerichtlichen Gutachtens.) J. Hampe (of Brunswick), Klinik 
f. psych, u. nerv. Krankhciten, Bd. 11, H. 1, 1907. Carl 
Marhold, Halle a. S. 

In this paper Dr Hampe discusses at considerable length one of 
those cases, frequently before the bar of justice, where the re¬ 
sponsibility of the accused is difficult to determine, where facts 
and arguments which appear cogent to the psychiatrist are dis¬ 
missed as unimportant or irrelevant by the jurist, cases for which 
the law does not as yet make adequate provision and in which a 
just sentence—or what seems so to the mental expert—can only 
be obtained by an elastic, and to the legal mind unwarrantable, 
interpretation of the law. 

Briefly the main facts are as follows:—S. the accused, who 
had already served one or two terms of imprisonment, was tried 
at the Assizes for peijury, having given false witness during the 
trial of his son for the assault of a man with whom both father 
and son were at enmity. Doubts as to his sanity were entertained 
during his remand whilst awaiting trial, but no prison officials 
were called to give witness, and although similar doubts had been 
expressed on a former sentence in 1884, evidence of this was 
ruled out as inadmissible through the death of the persons con¬ 
cerned. At the trial the following facts were elicited: hereditary 
influences (mother demented, second son weak-minded); S. himself 
a sober, industrious, and on the whole well-behaved man, but from 
childhood somewhat simple and below the average mentally ; 
thirteen years before this trial, head-trauma with loss of conscious¬ 
ness, followed by various nervous symptoms, headache, depression, 
insomnia, impaired memory, at times thoughts of suicide, and 
periodic fluctuations of emotional tone. Alcoholic intolerance is 
also asserted by Dr Hampe, but this apparently does not rest on 
an experimental basis. On bodily examination, apparently normal. 
Examination as to the psychical state showed marked intellectual 
incapacity, very deficient power of attention, incomprehension of 
abstract terms, including the meaning of “ perjury ”; and examina- 



tion by Ranschburg’s word-pairing method showed a paramnesia 
from frequent confusion of past with recent impressions. On the 
grounds of the above results Dr Hampe has no hesitation in in¬ 
cluding S. within the scope of § 51 of the Strafgesetzbuch. In the 
absence, however, of specific delusions or hallucinations, the 
necessity for whose presence seems to obsess the legal mind, S. 
was sentenced to five years’ penal servitude. 


HESSE. (Vereinigung fiir gerichtliche Psychologic und 
Psychiatric im Grossherzogtum Hessen. ) Juristisch-psychiatruche 
Gremfragen, Bd. 5, H. 6. Carl Marhold, Halle a. S., 1907 r 
pp. 66, price M. 1.20. 

This report of the proceedings at the above congress, held under 
the presidency of Attorney-General Dr Preetorius of Darmstadt at 
Butzbach last July, is composed of two parts: the first dealing 
with a discussion upon the organisation of courses of lectures upon 
penology for jurists ; and the second with the function of medical, 
and particularly of alienist, experts in the witness-box. The dis¬ 
cussion on the organisation of lectures on penology (Gefangnis- 
lehrkursen) was opened by Professor Mittermaier of Giessen, who 
strongly maintained that such courses should not only include 
lectures on penological principles, on psychology, anthropology, 
sociology, and statistics, as theoretical subjects from the special 
point of view of criminology, but also a practical course. The first, 
the theoretical, appertained to the University, but the practical 
course could only be carried out in the prison, wherein not only 
the conditions of actual punishment could be studied, but the 
criminal himself. The following speakers were in substantial 
agreement with Professor Mittermaier, and the resolution was 
passed that, subject to the consent of the Minister of Justice (Lord 
Chancellor), courses (in penology and criminology) should be 
inaugurated in Hesse for jurists and medical men in the service of 
the State; the practical course to consist of ten to fourteen days a 
year, and to be conducted at the central prison of Butzbach and 
Marienschloss, preceded by theoretical instruction. 

Such practical instruction is already given at Baden (since 1886), 
in Prussia (since 1895), in Bavaria (since 1900), and in Hambuig 
(since 1904), and there seems to be no reason why it should be 
limited to these places, or indeed to Germany, for there can be no 
doubt, as Professor Mittermaier said, that an intimate knowledge 
of the factors of crime can be gained more easily and completely 



in the prison than in the law courts; that an acquaintance with 
the conditions and effects of punishment—surely indispensable to 
the judge—can be acquired only in the prison ; and that the prison 
affords opportunities for such study of the working of the criminal 
mind as would be invaluable to those who have to settle the 
question of the responsibility or irresponsibility of persons accused 
of crime. This leads at once to the questions : Who have to settle 
the responsibility or the irresponsibility of the accused? and. 
What is the place and function of the medical witness, and in 
particular of the alienist expert ? As to the former question, the 
law as it stands, in Germany as in England, admits of no doubt. 
The settlement of the responsibility or irresponsibility of an 
accused person rests with the judge and jury and never with the 
medical expert. This was of course the view of Professor 
Mittermaier, who introduced the discussion, Die Tatigkeit des 
MediziniscJien, im besondem des psychiatriscJien Sackverstdndigen 
vor Gericht, and this was acquiesced in by all the subsequent 
speakers, including Professor Sommer, who restricted his remarks 
to a criticism of existing practices as to the preparation and fram¬ 
ing of evidence for judgment He stated, however, that, since the 
time when the laws were formulated, concepts as to what con¬ 
stituted irresponsibility have largely altered, and that the law 
should be interpreted in the light of modern information, i.e. should 
regard the results of minute psychological inquiry into the total 
personality of the individual and, by implication, the extension of 
the protective clauses (§51, Str. G.-B.) 1 to persons not strictly and 
legally within their scope, or who were not considered so when the 
laws were framed. It is evident, however, that if this question of 
responsibility is one solely for the jurist, as it undoubtedly is at 
present in legal courts, and if the expert evidence is to be rigidly 
confined to facts and not to include expert decisions, then the jurist 
must be in a position to appreciate the bearing of every one of 
these facts; that is, he must be instructed in psychiatry. This is 
the position taken up by Professor Sommer, who prophesies that in 
the near future “a certain psychiatrical knowledge will be 
obligatory upon the jurists,” in support of which he refers to a 
recent ministerial order. R. Cunyngham Brown. 

1 § 51 of the DeutseJus Strafgesetzbuch runs as follows : “ Eine strafbare Hand- 
lung iat nicht vorhanden, wenn der Tater zur Zeit der Begehung der Handlung sich 
in einem Zustande von Bewusstlosigkeit oder krankhafter Stoning der Geistestatigkeit 
befand, durch welchen seine freie Willensbestimmung ausgesohlossen war." 




(187) IN GERMANY SINCE 1902. (Weiterentwicklung der fiuni- 
jjgren Ver plleg qn g der jrr».wir<rimrig wn in Deutschland eeit 
1902.) Konrad Alt. Carl Marhold, Halle a. S., 1907, p. 16, 
price 76 Pf. 

In this short paper contributed to the International Congress of 
Alienists held at Milan in September last, Professor Konrad Alt, 
the well-known director of the great institution for the insane at 
Uchtspringe, Saxony, gives a comprehensive account of the growth 
of the family-care system in Germany in recent years. This 
growth, though rapid, will not appear surprising to those who are 
conversant with the admirable family-colony system which mostly 
obtains in Germany. The figures which Professor Alt gives speak 
for themselves. Whereas in 1882, in the whole of Germany, there 
were only two family-colonies, with about 50 boarded-out insane, 
in 1902 the colonies had increased to 32, with about 1200 patients. 
Since that time the proved value of this mode of disposal of the 
insane, both as a means of treatment and as a pecuniary gain, has 
won for it the confidence of both alienists and administrative 
authorities, with the result that, since 1902, the family-care 
system has been adopted as an auxiliary to asylum treatment at 
19 new centres, the insane so treated have risen to 2400 in 
number, and fresh developments are everywhere under considera¬ 
tion. Professor Alt’s survey is accompanied by a map of Germany 
showing the distribution of the family-colonies in Germany, and 
a chart showing graphically the growth of the boarded-out insane 
in Saxony in the decennium 1896-1906, showing a slow increase 
in number from 2 in January 1896 to 51 in 1900, and a rapid 
rise from that date to 475 on January 1 , 1906. Attention need 
be drawn to only one other part of this paper. Medical super¬ 
intendents in this country have occasionally expressed the opinion 
that the withdrawal of the well-behaved and able-bodied patients 
from the asylum to the outer colony must seriously affect the 
working capacity of the asylum. The same fear, Professor Alt 
says, has been expressed by some writers in his country, but his 
ten years’ experience has convinced him that the system does not 
necessarily entail any such result. The patients sent to family- 
care need not be composed only of good workers. Many who are 
idle in the asylum work cheerfully under family-care, and the 
withdrawal of numbers of good workers from the asylum at 
Uchtspringe has never permanently lowered the asylum output 
of work, the vacancies always being filled up by the remainder, 
even though previously unemployed. The point is of purely 
fiscal importance, for obviously the asylum exists for the insane 



and not the insane for the asylum, and experience has abundantly 
shown that the asylum plus the colony is much more economical 
than the asylum alone. R. Cunyngham Brown. 


logico del liquido cefalo-rachidiano nolle malattie men tali.) 

Pegna, Ann. di Nevrolog., f. 4, 1906, p. 241. 

The writer, in an article extending over 50 pages, quotes many 
authors to show that a lymphocytosis is a diagnostic feature of 
general paralysis, and he himself studies 65 cases of insanity, 
including 12 of this disease, which confirm this view. He further 
brings out a fact of the greatest importance in proving that the 
cerebro-spinal fluid of general paralytics is toxic to guinea-pigs. 
He divides his cases into three groups and subjects them to a series 
of examinations which comprises the specific gravity, cryoscopic 
index, percentage of lymphocytes and of serum globulin, presence 
or absence of serum albumin, negative bacteriological findings and 

Groups 1 and 2 contain 46 cases of all varieties of insanity, 
including epileptics. From examination of these he concludes 
that in no variety of insanity is there lymphocytosis except 
where there is a history of syphilis, and then it is only “ discrete,” 
i.e. only few cells present. The cerebro-spinal fluid is toxic to 
guinea-pigs only in the case of epileptics while suffering from fits, 
and the toxity is proportionate to the severity and duration of the 

Group 3 consists of 7 cases of senile dementia and 12 of general 
paralysis, and in these he found a trace of serum albumin in the 
former when arterio-sclerosis was present. While in general 
paralysis lymphocytosis always exists at some stage of the disease, 
serum albumin is present in varying amount according to the 
number of lymphocytes. The percentage of serum globulin is 
always high, and the specific gravity is increased (1009-1010). 
The cryoscopic index varies much in general paralysis, but is as a 
rule much lower than in other forms of mental disease. 

The effect of general paralytic cerebro-spinal fluid on guinea- 
pigs was very pronounced, varying in intensity with the proximity 
of congestive seizures. The inoculated animal died always within 
ten hours, and in one case in half an hour. 

The author emphasises his conclusions in an interesting 
summary. He states that a lymphocytosis of fifty to ninety 
in the cerebro-spinal fluid means an organic affection of the 
nervous system involving the meninges, and so serves to distinguish 
it from functional disorder, with a precision which cannot be done 



by any other known clinical method. A negative result doesn’t 
exclude general paralysis, but in the absence of lymphocytosis one 
would make a diagnosis of the disease with the greatest circum¬ 
spection, since it is usually one of the first signs of the malady. 
Cases of insanity in which there is a history of syphilis may 
show a lymphocytosis, but only in a very minor degree. 

The cryoscopic index in cases of general paralysis is usually 
low. The high percentage of serum globulin and the presence of 
serum albumin are valuable diagnostic indications. 

Toxicity of the cerebro-spinal fluid to guinea-pigs, inoculated 
with a quantity (five per cent, of body weight) of the material, is 
diagnostic of general paralysis, except only in cases of epilepsy 
during an accession of fits. Douglas M‘Rae. 

(189) ( Beschaeftigungstherapie fiir Nervenkranke.) Laehr, JViener 
kl. Wochenschr ., Dec. 27, 1906. 

In this paper the writer discusses the practical value of the treat¬ 
ment of cases of nervous disease by means of work, and gives the 
results of six years’ experience as director of a sanitorium near 

He discusses what is meant by the term “ work,” and decides 
that the criterion of suitable work is that the person shall feel 
happy in doing it. After such work the most lasting and intense 
change of mood takes place; and, generally speaking, the proper 
work is of a physical nature. This form of treatment, he states, 
adapts itself to any form of neuropsychosis, whether manifesting 
itself as neurasthenia, hysteria, or hypochondriasis, and is specially 
suited for traumatic cases. Two primary conditions must be present, 
however: that the patient must feel ill and wish for treatment, 
and that he must have no insuperable disinclination to work. 
The quickest and best result is obtained, he says, from those 
patients who realise most fully the importance of the work for their 
bodily and mental improvement. Contra-indications for the treat¬ 
ment are an acute condition of exhaustion, toxic conditions, weaken¬ 
ing diseases, some injuries, and great overstrain. 

As to the nature of the work, he believes that manual work 
of a purposive character in the open air is most suitable for all 
classes. Above all, he recommends carpentry and gardening; 
for weaker persons bookbinding, cardboard work, and wood-carving ; 
sometimes drawing, painting, or photography; and for women 
various kinds of housework. With the patients there must be 
a skilful, sympathetic, and tactful supervisor, and the physician 
must carefully watch the effect of the work upon the patient. 

John D. Comrie. 




(190) la Scopolamine snr la Choree de Sydenham.) Babinski, Soc. 

de Neur ., Jan. 10, 1907, Rev. Neurol., p. 86. 

Bablnski has treated four chorea patients with hydrobromide of 
scopolamine given subcutaneously in doses from \ to £ mg. a day. 
The results were good in all cases; in one it was very striking as 
the disease was very severe and prevented sleep. 

Ernest Jones. 


(191) BIRTH PALSY. Alfred S. Taylor, M.D., Jonm. of the Am. 

Med. Ass., Jan. 12, 1907. 

Brachial birth palsy of the Erb type is due to overstretching of 
the nerve roots, resulting in rupture of the sheath and nerve fibres, 
haemorrhage between the tom fibres, and resulting cicatrisation 
which prevents transmission of nerve impulses. Nerve conduction 
can be re-established only by excision of the cicatricial area or 
areas, and end-to-end suture of the nerves. The nerves involved 
having been ascertained before operation, the brachial plexus is 
exposed at the lower part of the posterior triangle of the neck; 
the adherent fascia is dissected off, the indurated portions of the 
nerves removed, and the healthy ends joined by suture, or, if the 
gap is too great for this, by means of a catgut bridge. Though the 
suprascapular nerve is small, it must receive special attention, as 
it supplies the external rotator muscles of the shoulder, whose 
paralysis causes the marked internal rotation of this paralysis, as 
well as the tendency to posterior dislocation of the shoulder. 

Early operation—between six and twelve months if possible— 
is indicated. Delay results in impaired development of the 
extremity, contractures of muscles and ligaments, and atypical 
shape of the joint-ends of the bones, all of which diminish the 
chance of operative success. Massage, electricity, and passive 
movements must be employed to prevent these deformities both 
before and after operation. Generally additional muscles are at 
first paralysed by the operation, as some normal nerve fibres are 
necessarily divided; but this operative paralysis has often com¬ 
pletely disappeared within six or eight months. Improvement in 
nutrition and development of the limb usually begins in four 
months, and return of power in the originally paralysed muscles 
appears in from six to ten months. The author has operated upon 
nine cases. Two died from causes not inherent in the operation 
itself. One case, in which nerve-bridging had to be employed, 
showed trophic disturbances of the fingers, which comparatively 
soon disappeared. All the cases which recovered show consider¬ 
able and progressive improvement both in development and 
function. W. J. Stuart. 




A TEXT-BOOK OF PSYCHIATRY. Leonardo Bianchi, Professor 
of Clinical Psychiatry and Neuropathology in the Royal 
University of Naples. Translated from the Italian by James 
H. Macdonald, M.B. Pp. 877. London: Baillifere, Tindall & 
Cox. 1906. 

This is a lengthy volume, of which, roughly, nearly one-half is 
devoted to a description of cerebral anatomy—macroscopical and 
microscopical — and physio-pathology. The remaining larger 
portion deals with clinical psychiatry. As a matter of experience 
we think that this combination of the two subjects in one book, 
however important their bearing the one upon the other, is a 
mistake. The modern student, driven by the force of a stupendous 
pressure to systematise knowledge and to acquire facts, has neither 
the time nor the inclination to sit down to the study of a com¬ 
pendium embracing at once everything that can possibly be known 
about one system of the body; he likes his information in depart¬ 
ments ; if clinical, then he applies to a clinical work ; if physio¬ 
logical, he prefers the laboratory or a work by a physiologist. It is 
the same with the busy physician. 

The work of Professor Bianchi upon the sciences cognate to 
and introductory to psychiatry are so well known, and his erudition 
and research are so well established, that the first portion of this 
work need not detain us at the present time. It contains a 
treasury of useful information, luminously presented and inclusive 
of most of the facts which a student of neuro-physiology and neuro¬ 
pathology requires in his reading. The direct bearing of these 
facts upon the teaching of clinical psychiatry has not as yet been 
by any means established. This is not stated by way of reproach 
to our author, but as an unfortunate though irrefutable fact. 

The part of the book devoted to the description of mental 
diseases is very clearly written, and contains much valuable 
information which, moreover, bears the unmistakable stamp of 
originality and of long and patient observation. It is unfortunate 
that the usefulness of the book as a work of reference is somewhat 
curtailed by the want of any definite line of classification, and 
occasionally by the use of a terminology which is alien to any 
recognised nomenclature in the literature of the subject. In his 
discussion upon classification, Professor Bianchi remarks that “ The 
two criteria in the formation of a scientific classification which 
have been so happily employed in general medicine would, if 
adopted in psychiatry, give a very inferior and confusing result. I 
allude to the aetiological and anatomo-pathological criteria.” It is 
strange that in this connection he neglects to mention the 
symptomatological criterion which is so happily combined in 



general medicine with the other two. Why should it not also 
be combined in psychiatric medicine ? In any case the author 
does not incline to adopt any classification, but contents himself 
by dividing all mental affections into three groups as follows: 
(1) Affections represented essentially by an evolutionary psycho¬ 
cerebral defect; (2) A group comprising all the mental affections 
of infective, autotoxic, and toxic origin developing in individuals 
regularly evolved; and (3) All mental infections with an organic 
substratum, localised or diffuse, in the central organ of mind. 
The scheme is ingenious and plausible, but a little consideration 
will show that the result cannot fail to be unsatisfactory owing to 
the incessant overlapping of the various members of the different 
groups. A cursory glance at the classification is apt to be 
bewildering in the extreme, for it reveals the close proximity of 
clinical entities which we have always been taught to regal'd as 
essentially distinct and unrelated. 

With regard to terminology, many points might be referred to, 
but one will be sufficient Professor Bianchi sets up a new clinical 
entity which he designates “ Sensory Insanity.” He tells us that 
he makes use of this name because in his experience the first 
symptoms of the disease invariably commence with sensory dis¬ 
orders (hallucinations or illusions). The initiated reader will 
perceive before he has read very far into this disease that he is 
dealing with Kraepelin’s Dementia Prtecox, every division of 
which is described and included. It is satisfactory to find two 
such distinguished physicians confirm one another’s clinical 
experiences. On the other hand, it is unfortunate for himself that 
Bianchi’s claim for priority is so hopelessly in arrear, although we 
confess that we should find it difficult to adopt his theory of 
sensory origin for the symptoms of this great group. 

Generally speaking, Professor Bianchi’s book is, as we should 
expect from the pen of so eminent a man, a perfect mine of new 
and instructive information, and if it is not arranged to suit the 
tastes of the British reader, we are willing to concede that that may 
be quite as much the fault of the Islander as of the Italian. 

In any case it is not the fault of the translator, who has devoted 
evidently a great amount of time and thought to presenting to the 
English-speaking reader, in commendably lucid language, the first 
great Italian work on mental diseases that has been translated 
into English. 


Benno Eonegen, Leipzig, 1906, price M. 1. 

This pamphlet of 26 short pages, which has been sent us for 
review, is one of a series dealing with the more important diseases 
of the nervous system, and written expressly for the general 
practitioner. Edwin Bramwell. 



proceedings of Societies 

At a meeting of the New York Psychiatrical Society, held on 
January 2, 1907—the President, Dr Adolf Meyer, in the Chair— 
a paper on “The Symptomatic-Prognostic Complex of Manic- 
depressive Insanity” was read by Dr George H. Kirby, of the 
Pathological Institute of the State of New York. Dr Kirby said : 
The field of psychiatry is too complex for us to expect absolute 
or clear-cut distinctions either in disease types or nosological 
groups. Kraepelin did a great service by showing that most of 
the previously made distinctions of types could be replaced by far 
more valuable nosological groups if one considered the whole 
course and outcome of mental disorders. From this point of view 
the great bulk of the acute psychoses can be brought under two 
divisions, viz. those that pass into deterioration and those that 
end in recovery. It was found that in cases which terminated in 
either of the above mentioned ways, one was able to identify certain 
characteristic symptoms present from the beginning , and which thus 
acquired a distinct prognostic value. Two large symptomatic- 
prognostic groups were thus created—Dementia Praecox and 
Manic-depressive Insanity. At present it seems best to consider 
the manic-depressive complex merely as a reaction type and not a 
disease entity as Kraepelin proposes. It is rather a type of re¬ 
sponse which may be elicited in various ways. In some cases the 
constitutional disposition may be most important, but in others 
the exogenous causes are of great importance and give valuable 
hints as to prophylaxis and probability of recurrence. This 
peculiar kind of reaction in its pure form has the characteristics 
of a benign disorder and thus a favourable prognosis is implied. 
Various additional elements may enter to confuse the picture, and 
the symptomatic and prognostic features may seem to diverge at 
various times. There are many equivalents difficult to recognise. 
In a few cases the principle seems to fail through transitions to 
other forms. 

A series of cases was reported which had offered difficulties for 
various reasons. Some patients were also presented. A recurrent 
depression with retardation and prominent auditory hallucinations. 
Another case of depression with sensory-somatic complex and only 
slight signs of difficulty in thinking. A third case illustrating the 
mixed forms of manic-depressive insanity, the so-called “ manic- 
stupor,” showing inhibition and mutism with an exhilarated mood. 


Dr Charles L. Dana was inclined to think'“ prognostic principle ” 
a rather unfortunate term, inasmuch as this was not all that was 
used in attempting to establish types. The consideration of the 



whole life history was the great principle to be used in making 
classifications, and he did not think there could be any objection 
found to basing groups of insanity upon this method. It was not 
new, but the rational and accepted one in other forms of disease. 
The case presented by Dr Kirby in which there was melancholia 
without retardation of thought was interesting, but was a type 
not infrequently seen outside of asylums at least, and often in con¬ 
nection with intense suicidal feelings. This suicidal impulse was not 
always due to somatic feeling of inadequacy, but was sometimes 
also a well reasoned out point of view. A woman of intelligence, 
for example, realising that she had had melancholia now for three 
times, that she would have it again, that she would be a burden to 
her family, that she would never be right permanently, schemes to 
kill herself, obeying in a way a logical conclusion as well as a morbid 
impulse. Such patients did not have always retardation of thought, 
but they often could not do their work easily or effectively. He did 
not believe the first patient presented by Dr Kirby would be able 
to do her work. Such patients could not play games of skill as 
formerly, becoming tired quickly. Dr Kirby had neglected to touch 
upon chronic melancholia, melancholia of involution, a group which 
Dr Dana believed to be represented in early life. He had records 
of cases of melancholia at the climacteric who gave a history of 
depression earlier very much like that of later life, so that there 
was a melancholia of early life which did not belong to manic- 
depressive insanity. 

Dr L. Pierce Clark thought the symptom-complex of manic- 
depressive insanity would be easier of analysis if the idea were 
borne in mind that the complex was likely to partake of the 
nature of the physiological epochs at which it occurred. The 
suicidal impulse to which Dr Dana referred was well known to 
most alienists. Even in convalescence this tendency was most 

Dr August Hoch said it was usually claimed that it was 
impossible to formulate any laws of prognosis about the different 
forms of manic-depressive insanity. This was not quite correct. 
Dr Kirby had shown that a careful reasoning might do much in 
formulating a special prognosis. Dr Hoch wished to mention a 
few more general points of view from which a prognosis might be 
made. The first referred to the depressions. The symptoms of 
the entire depressive complex were retardation, sadness, and the 
anxiety-unreality complex. In the typical manic-depressive states 
there were only sadness and retardation. In such cases the 
outlook was good. In the typical involution melancholias there 
was, from the beginning, uneasiness, anxiety, to which were often 
added later in the course symptoms of the anxiety-unreality 
complex. In such cases the outlook was bad; such patients got 
into a state of deterioration, characterised by a narrowing of the 



mental horizon. But the anxiety-unreality complex might also 
be reached by way of the manic-depressive states. This happened 
not infrequently in the manic-depressive depressions, which occur 
at the involution period, sometimes in those occurring earlier in 
life. These cases might, therefore, begin with a typical retardation 
or feeling of inadequacy, and then develop an anxiety-unreality 
complex. In such cases the prognosis was not so bad as in the 
typical involution melancholias, but decidedly less good than in 
the simple manic-depressive depressions. 

The second point of view referred to the prognosis of the 
manic states. All alienists knew that those cases which present 
the .best prognosis are cases of clean-cut manias of considerable 
intensity, manias in which the exhilaration, the general excitement, 
and the flight of ideas are all of about the same degree. The 
hypomanic states were much less favourable prognostically. Dr 
Hoch had always found that cases in which the disorder of 
behaviour was out of proportion compared with the flight of ideas 
and the intellectual disorder in general, were prognostically also 
more unfavourable. Such cases were apt to have long attacks or 
many attacks. The prognosis in wises in which a delusional 
element was strikingly out of proportion to the flight of ideas was 
also more doubtful than in the simple classical mania. In other 
words, the cases of mania in which there were strong discrepancies 
in the intensity of the different symptoms were those which 
presented a less favourable outlook than those in which there 
existed a certain harmony in the intensity. 

C. Mackie Campbell. 



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iLCMOL, ET€.— 

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Epilepsy.—W. ALDREN TURNER. Epilepsy : a Study of the Idiopathic Disease. 
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W. G. SPILLER. Psychasthenic Attacks simulating Epilepsy. Journ. Abnormal 
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Traumatic Neuroses.—.JULIUS BRAUN. Praktische Erfa h run gen uher die trail - 
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Tic.—MEIGE and FE1N«»AL. Tics and their Treatment. Translated by S. A. K. 

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tmiL 8EN8E8 A9D C1AM1U NEKVEfr— 

8ANDF0RD. The Means of fearly Detection of Affections of the Special Senses 
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VAUGHAN. Einige Bemerkungen uber die Wirkung von Santonin auf die 
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WEBER. Zur prognostischen Bedeutung dea Argyll-Robertson’schen Phenomena. 
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HERMANN SCHLESINGER. H orison tale Bulbusschwingungen bei Lidschluss; 
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MOSCHCOWITZ. The Radical Cure of Trigeminal Neuralgia by means of Peri- 

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[ARET, N6vralgie faciale et radio-therapie. PressemSd mars 13, 1907, p. 162. 
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p. 169. 

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p. 160. 

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Mv. 1, 1907. 

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Neurol., mars 5. 1907, p. 86. 

PIERRE MARIE et FRANCOIS MOUTIER Un nouveau caa d'aphasie de 
Broca dans lequel la troisifeme circonvolution frontale gauche n'eet pas atteinte, 
tandis quo la ramollissement occupe la tone de Wernicke et les circonvolutio as 
motricea. Bull, de la Soc. mid. dee h6p. de Pam, f6v. 15, 1907. 

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p. 117. 

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Bd. 21, H. 3, 1907, S. 248. 

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Falles von einseitiger Apraxie. Centralhl. f. Nervtnkeil%. «. Psychiat ., M&rz 1, 
1907, S. 161. 


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Baillifere et fils, Paris, 1907, fr. 1.50. 

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Neurol., f6v. 28, 1807, p. 137. 

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Stuttgart, 1907, M. 3.60. 

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in anderer psychisch-norvosor Leiden. Webel, Leipzig, 1907, M. 3. 

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oder die Suggestion und Psychotherapie. Enke, Stuttgart, 1907, M. 6. 

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1907, p. 665. 

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larynyol. et de rhiuol., mars 16, 1907, p. 305. 

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Individual Diseases. 


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K. Wilson. Sidney Appleton, London, 1907. 9s. 


will be held at Amsterdam on the 2nd to 7th September 1907, under the 
patronage of Her Most Gracious Majesty Queen Wilhelmina and of His 
Royal Highness Prince Hendrik of the Netherlands. The Congress will be 
divided into two parts : General Sessions and Meetings of Sections. In the 
former, chosen subjects will be dealt with by competent men who have been 
invited for that purpose ; in the latter, questions will be discussed and 
criticism will be invited. Anyone taking an interest in Psychiatry, Neuro- 
logy, Psychology, and the Nursing of Lunatics may become a member of 
the Congress. Those wishing to attend the Congress are requested to 
communicate with the General Secretary, Prinsengracht 717, Amsterdam. 



IReurolog^ anb ifrs^cbiatrp 

Original articles 

TEM . 1 

By Dr ORR, 

Pathologist, County Asylum, Prestwich ; 


Pathologist, County Asylum, Lancaster. 

In a previous paper (1) we described the lesions in the posterior 
columns of the spinal cord in general paralysis, and pointed out 
their similarity with those in early tabes dorsalis. Our con¬ 
clusion with regard to the starting-point of the degeneration was 
that it commenced in the intramedullary portion of the sensory 
fibres immediately the neurilemma sheath was lost. It is im¬ 
portant to clearly differentiate this point from that at which the 
posterior roots undergo a constriction on passing into the cord, 
as they do not coincide ; in fact in the region most usually con¬ 
cerned in tabes (lumbo-sacral) the neurilemma leaves the fibres at 
a point situated outside the constriction (2). Nevertheless we 
would speak of the nerves as intramedullary as soon as they lose 
Schwann’s sheath. 

During these observations on the sensory fibres, in which it 
was apparent that the absence of neurilemma played an im¬ 
portant part in the localisation of the onset of the lesion, we 

1 Towards this research the British Medical Association has assisted by a grant 
of money. 

R. OF N. & P. VOL. V. NO. 6—Z 



naturally inquired into the condition of the intramedullary 
portion of the motor nerves, but found the changes in these as a 
rule difficult to trace. We therefore extended our investigations 
to the cranial nerves, and found that the lesions began in both 
sensory and motor roots at a point which corresponds to that 
already indicated in the spinal nerves; and the changes found 
therein form the first part of this paper. 

While our attention was still confined to the posterior 
columns of the cord we had indications of the advisability of 
inquiring into what was already known of their lymphatic sys¬ 
tem, and we obtained evidence of a continuous flow of lymph 
upwards along the nerves, and that the main current lay at the 
periphery of the nerve bundles immediately under the fibrous 
sheath. References to the authors holding this view have been 
given in our previous publications, so that here a short re¬ 
capitulation will suffice. It is well known that tetanus and 
rabies spread to the cord by the nerves ; and in this connection 
we might mention the experiments of Marie and Morax (3) who, 
after cutting the nerve to the fore limb of an animal and later 
injecting a lethal dose of the tetanus toxin into the paw, found 
that no convulsions followed. Hom4n and Laitinen (4), after 
injection of streptococci into the sciatic nerve, traced the 
organisms upwards into the meninges of the cord; while Pirrone 
(5), experimenting with the pneumococcus, found changes in the 
cord, but limited to the side corresponding to the nerve injected. 
In addition to organisms, chemical and inert substances have 
been used with like results, e.g. Guillain (6) injected ferric 
chloride into the sciatic nerve, subsequently introducing potas¬ 
sium ferrocyanide into the general circulation, and found Prussian 
blue in the posterior roots. Sicard and Bauer (7), using China 
ink, observed, after injection into the nerve, that the granules 
ascended along it towards the cord. It was presumable there¬ 
fore that, if these views were correct, we ought to find in the 
cord of cases in which some septic focus existed, lesions of the 
posterior columns caused by toxins ascending in the lymph 
stream. On examining cases of brachial neuritis (infective), bed 
sores, suppurating knee-joint, septic psoas abscess, we found, in 
the cord of all, the lesions expected. These also commenced at 
the vulnerable point above indicated, and resembled in their 
distribution early tabetic degenerations (8). 


Bearing these facts in mind, the question of a possible lympho¬ 
genous infection of the central nervous system seemed worthy of 
farther investigation, owing to the apparent facility with which 
toxins gained access by the nerves ; and it was with a view to 
testing this that our experiments were conducted. Besides, 
apart from the question of etiology, the introduction of toxins by 
the nerve lymph paths promised, if successful, to offer a con¬ 
venient means of inducing cord and cranial nerve lesions, and to 
afford one the opportunity of studying them in their early 
phases. We have already published a series of clinical cases 
(1 and 8) showing the lesions found in the spinal cord in general 
paralysis and in other toxic conditions, and before giving the 
results of our experiments we submit the following cases illustra¬ 
tive of lesions of the cranial nerves. 

Lesions of Cranial Nerves in Toxic Conditions. 

Clinical Cases. 

Case 1.—An ataxic general paralytic. The first symptoms were noticed 
about three years before his death. 

Examination of the pons and medulla showed the following lesions of the 
cranial nerves ;— 

Third Nerve .—Both third nerves were affected to a slight degree. By the 
Marchi method the degeneration was exhibited in the form of small, round, 
black globules, which could be followed along the nerve fibres from the 
periphery almost to the nucleus of origin. 

Fourth Nerve .—The left fourth nerve was affected much more than the 
right In the latter, globules were present, as in the third nerve, but were 
larger. In the left nerve the degeneration was in the form of larger and 
more irregular masses, which were arranged in series along the nerve fibres. 
They could be traced from the point where the fibres lost their neurilemma 
sheath—and the lesion was most intense in this region—to the nucleus of 
origin. There was no degeneration in the fibres outside the pons. 

Fifth Nerve .—The left fifth nerve showed more degeneration than any 
other cranial nerve, and exhibited many interesting changes ; the right was 
also affected, but to a less degree. Immediately beyond the point where the 
fibres had lost their neurilemma sheath (Photo 4), an intense lesion was 
found, which by a low power seemed to consist of large irregular masses 
arranged in rows. But with a higher power the changes were seen to be of 
different types. In some fibres there were series of large irregular masses 
similar to those which are characteristic of Wallerian degeneration; in other 
fibres the reaction assumed the form of black sinuous threads (see Photos 
1 and 3); in some, round or oval globules of various sizes were seen, and 
some fibres showed no Marchi reaction at alL 

These various types of degeneration indicate different degrees of injury to 



the fibres. We are thus able to explain the fact that the degeneration was 
continued along many of the fibres of the descending fifth root, even as far as 
the first cervical segment (Photo 6). In the case of these fibres there must 
have been a necrosis of the axis-cylinder, as well as of the myelin sheath, 
immediately inside the point where the fibres lost their neurilemma sheath, 
which would produce a Wallerian degeneration in the portion of the fibres 
beyond the point of injury. In the descending root, however, there were 
many fibres which showed no degeneration, and these would correspond to 
the unaffected fibres, which were seen in the first part of the intracranial 
portion of the fifth nerve, and also to those fibres which exhibited the slighter 
degrees of change. 

In the right fifth nerve round and oval globules were present, but there 
was no evidence of any necrosis such as was met with in the left nerve. 
Corresponding to this there was an absence of degeneration amongst the fibres 
of the right descending root. 

Sixth Nerve. —In both sixth nerves there was considerable degeneration 
demonstrated by the Marchi method. Here the thread-like form was more 
in evidence, accompanied by many round and oval globules. 

Seventh and Eighth Nerves. —In these nerves very little degeneration was 

Ninth and Tenth Nerves. —On the left side there were many affected fibres 
in which the degeneration could be traced from near the periphery of the 
medulla oblongata to the fasciculus solitarius. In the right nerves there was 
little change. 

Eleventh Nerve. —The right nerve in this case showed a marked lesion, 
which could be followed from the periphery to its nucleus. 

Twelfth Nerve. —There was practically no lesion of the fibres of the twelfth 

In this case it was evident, from the appearances found, that 
an acute degenerative process had supervened on a chronic 
morhid condition. In the ninth and tenth nerves especially 
there was evidence that a slow atrophy had taken place, par¬ 
ticularly near the border of the medulla oblongata. But in the 
left fifth nerve, and to a less extent in the left fourth and both 
sixth nerves, the increase in the amount of the Marchi reaction 
and the presence of the large, irregular masses, and the fact that 
the degeneration in the fifth could be followed from the edge of 
the pons along the fibres of the descending root of the nerve to 
the first cervical segment, indicated an acute degenerative 

Case 2. —Melancholia. At the post-mortem examination a tumour waa 
found in the anterior part of the left lobe of the cerebellum ; there was also 
an acute basal meningitis, which was more marked on the left side of the 
pons and medulla. In this case the third nerves were not examined. 


Fourth Nerve, —Both fourth nerves showed some degeneration which could 
be followed from the point where the fibres pierced the pia mater to the 
nucleus of origin. Most of the Marchi reaction was seen in the form of round 
or oval droplets, but the thread-like type was frequently present 

Fifth Nerve .—The maximum intensity of the meningitic process was at 
the level of the left middle cerebellar peduncle, and the cranial nerves which 
were nearest to this region showed most degeneration. 

The fifth nerves were both affected, but in the left nerve most of the 
fibres showed an acute degenerative reaction. This was seen chiefly in the 
form of round or oval globules of various sizes ; but with this there was also 
some thread-like degeneration, and in some fibres the affected myelin lay in 
larger and more irregular masses. 

Some degeneration could be traced to the motor nucleus. 

In this case, however, although there was such an intense degeneration in 
the fibres of the left nerve, only a small number of affected fibres were present 
in the descending fifth root 

Sixth Nerve .—Some Marchi reaction, in the form of round globules, was 
present in both sixth nerves. 

Seventh and Eighth Nerve* .—The seventh and eighth nerves on the left side 
showed considerable degeneration, but the right nerves were affected to only 
a slight degree. 

On the left side the degeneration could be followed from the periphery of 
the pons to the nucleus in both nerves. In the seventh nerve there was 
some thread-like degeneration, associated near the periphery with some 
larger irregular masses; but in the other parts of this nerve and in the 
eighth the reaction consisted chiefly of round or oval globules of various 

Ninth, Tenth, and Twelfth Nerve a.—In all these nerves, globules of Marchi 
reaction were present. In the left tenth nerve the degeneration could be 
traced from the periphery around the fasciculus solitarius to the nucleus 

In this case the most important fact to be observed is that 
the degree of the lesion varied with the intensity of the menin¬ 
gitic process. This was most marked at the level of the middle 
cerebellar peduncle, especially on the left side, and it was in this 
region that the cranial nerves were most affected; in fact, those 
connected with the lower portion of the medulla, where the 
meningitic changes were scanty, exhibited only a slight degree of 
degeneration. The lesion of the left fifth nerve was very acute, 
as shown by the character of the Marchi reaction, but there were 
few degenerated fibres in the descending fifth root; there can be 
little doubt, however, that if the process had lasted a little 
longer, necrosis of the axis-cylinders and myelin sheath would 
have been produced, and there would have followed a Wallerian 



degeneration of the fibres extending throughout the descending 

At the same time it is interesting to find that the lesions in 
the fibres began at the same point, viz. immediately they had 
lost their neurilemma sheath, and that they were of the same 
character, as in cases where the septic focus was extra-cranial 
(see infra). 

Case 3.—General paralysis. Gait markedly ataxic. 

Cranial Nerves. — Third and Fourth Nerves. —Some degeneration present in 
the form of round droplets. 

Fifth Nerve. —Both fifth nerves affected to a considerable extent. Descend¬ 
ing root nil. 

Sixth Nerve. —Considerable degeneration. 

Seventh and Eighth Nerves. —Slight degeneration. 

Tenth and Twelfth Nerves. —Very slight degeneration. There was consider¬ 
able degeneration in both superior cerebellar peduncles. 

Case 4.—Melancholia. Cause of death—General tuberculosis. Suppura¬ 
tion of the mastoid cells on both sides. 

Cranial Nerves. — Third Nerve. —Some degeneration. 

Fourth Nerve. —Considerable degeneration. 

Fifth, Sixth , Seventh, and Eighth Nerves. —Much degeneration in all these 
nerves on both sides. Threadlike, round, and large irregular types present. 

Case 5.—General paralysis. 

Cranial Nerves. — Third and Fourth Nerves .—Very little degeneration. 

Fifth Nerve. —Only one fifth nerve showed much degeneration. 

Sixth Nerve. —Maximum degeneration. Both nerves affected. 

Seventh Nerve. —Considerable degeneration on both sides. 

Eighth , Ninth, and Tenth Nerves. —Little degeneration. 

Twelfth Nerve. —Some degeneration on both sides. 

Case 6.—General paralysis. 

Cranial Nerves.—Third and Fourth Nerves. —Slight degeneration. 

Fifth Nerve. —Considerable degeneration of the peripheral type, i.e. the 
degeneration was found only in the peripheral portion of the myelin sheath, 
the rest of the fibre showed no change. 

Sixth and Seventh Nerves. —Considerable degeneration in the form of round 

Eighth Nerve. —Some degeneration of the peripheral type. 

Tenth and Twelfth Nerves. —Very little degeneration. 

Case 7.— General paralysis. 

Third and Fourth Nerves. —Practically no degeneration. 

Fifth and Sixth Nerves. —Considerable degeneration on both sides. 

Seventh and Eighth Nerves. —Slight degeneration. 

Ninth , Tenth, and Twelfth Nerves. —Practically no degeneration. 


Case 8.—General paralysis. 

Necrosis of skin over the right shoulder, muscles bare, pus burrowing 
amongst muscles, abscesses in the right trapezius. Very little degeneration 
in any cranial nerve excepting the eleventh on the right side. 

Case 9. —General paralysis. 

Some changes in the sixth, seventh, and eighth cranial nerves. Practically 
nil in the others. 

Case 10.—General paralysis. 

There was an acute degeneration in one fifth nerve. Practically nil in the 
other cranial nerves. 

In this series of ten cases in which the cranial nerves were 
examined there are a few points to which we wish to draw 

The series included eight cases of general paralysis, one of 
tumour of the left lobe of the cerebellum in which an acute 
basal meningitis was the ultimate cause of death, and one case 
of general tuberculosis. In the last-mentioned and in one 
general paralytic a septic process was present during life which 
seemed to have a direct causal relation with the lesion found 
in the cranial nerves. In the case dying of general tuberculosis 
this consisted of chronic middle ear and mastoid disease, and the 
maximum lesion was found in the seventh and eighth nerves, 
although there was considerable change in the sixth, fifth, and 
fourth nerves. In the general paralytic there was necrosis of 
the skin over the right shoulder, with abscesses in the deep 
muscles of the neck, and especially in the trapezius. The right 
eleventh nerve showed considerable degeneration, but in the 
others there was little to be found. 

In the remaining cases, in which no septic focus was found, 
the nerves connected with the pons, fifth, sixth, seventh, and 
eighth were more frequently and more seriously affected than 
those connected with the medulla oblongata. Again, the lesion 
commenced where the fibres lost their neurilemma sheath, and 
was of precisely the same character in motor and sensory nerves, 
and in no nerve was there any recognisable change in its 
extra-pontine portion. 

The next point to be considered is the character of the lesion, 
as exhibited by the Marchi method. All degrees of degenera¬ 
tion were seen. The most intense was that in which there had 
been a necrosis of the axis-cylinder and of the myelin sheath 



in the left fifth nerve of Case 1, with consequent Wallerian 
degeneration, which could be followed in the descending fifth 
root to the first cervical segment of the spinal cord. 

The other forms in which the degeneration was seen were 
(a) the slender moniliform thread, (b) the peripheral type in 
which the portion of the myelin sheath farthest from the axis- 
cylinder was affected and the remainder of the fibre showed no 
change, and ( c ) the type which consisted of small, scattered, 
round or oval globules. As to the significance of these various 
types it is impossible at present to speak with certainty, but 
in all probability they depend upon the intensity of the 
degenerative process. It should be mentioned that even in the 
most acute cases, side by side with the fibres showing signs of 
intense lesion, lay others in which no sign of degeneration was 
demonstrated by the Marchi method. 

The last point to be mentioned is, that in several of the 
chronic cases the evidences of degeneration were most marked 
at a little distance inwards from the periphery of the pons or 

This condition is present to a certain extent in most chronic 
cases, and was well seen in the tenth nerve of Case 1, who was a 
general paralytic of three years’ standing. Further examination 
of this condition, by Medea’s modification of Mann’s method (9), 
demonstrated that although the axis-cylinders could be traced 
from the point where they pierced the pia mater, no myelin was 
present around them for some distance inwards. Evidently in 
these chronic cases a slow atrophy of the myelin takes place in 
the portion of the fibres most exposed to the attack of some weak 
toxin which approaches along the perineural sheath of the nerve. 
This may proceed until the axis-cylinder is laid bare, and there¬ 
fore, as all the myelin in this peripheral portion of the fibre has 
disappeared, there is nothing left to give a Marchi reaction. 

Toxic Lesions of the Spinal Cord and Cranial Nerves 
produced Experimentally. 

At the suggestion of Professor Lorrain Smith, in whose 
laboratory the experiments have been conducted, we adopted 
the following method. Celloidin capsules were filled with a 
broth culture of a certain organism, then sealed and laid along- 


side the exposed sciatic nerve, after which tne gluteal muscles 
were stitched in place and the wound closed. As toxins are 
known to diffuse through the wall of these capsules, we assumed 
that they would find their way into the ascending lymph stream 
of the nerves and so to the cord, where their presence would be 
demonstrated by the ensuing degeneration. The organisms we 
first employed were staphylococcus pyogenes aureus, bacillus 
pyocyaneus, Gaertner’s bacillus, and the bacillus coli; later we 
used the organisms taken from cases of acute colitis. We 
commenced our experiments at the beginning of 1905 and at 
first used organisms whose virulence had not been raised in any 
way. We found, however, that in order to obtain definite 
lesions it was necessary to do so, and further, that it was ad¬ 
vantageous to renew the capsule from time to time in order 
to maintain the supply of toxin. We purposely ignored at this 
stage the question of the predilection of certain organisms for 
the nervous system, and kept strictly to our original intention of 
confirming our own views and those of others on the direction of 
the lymph stream in the spinal roots, and the possibility of cord 
infection by this channel. 

Five successful experiments have been examined by the 
Marchi method; three on the cord and two on the pons and 
medulla. In the latter the capsule with its bacteria was 
implanted under the skin of the cheek, and the result of these 
two experiments has been to demonstrate certain special changes 
which occur in the intramedullary portion of nerves, especially 
motor nerves, in toxic conditions. The pons and medulla were 
cut in serial section in their entirety, and we eliminated as far 
as is possible the artefacts of injury incidental to the autopsy, 
by merely removing the bony covering and hardening in situ for 
one week in formalin 10%. Later the tissue was immersed in 
2% potassium bichromate before treatment with the Marchi 
method. Control experiments with capsules containing sterile 
broth were also performed. These yielded negative results. 

In the following description it has been necessary to go into detail, especi¬ 
ally with regard to the cranial nerves, as in each of these the degeneration 
varied in intensity as well as in type, for reasons at present difficult to under¬ 

Rabbit 1.—Capsule under Skin of Cheek.—Third Nerve .—This nerve was 
degenerated in its entire intramedullary course from its point of emergence 
back to the nucleus of origin, towards which, however, the changes were less 



marked. The myelin sheath showed as long, thin, black threads, with monili¬ 
form swellings at intervals, marking out the path of the nerve in parallel or 
sinuous lines (Photo 1). 

Fourth Nerve .—The degeneration here was much less than in the third 
nerve. There were sinuous filaments of altered myelin, but these were short, 
and situated only at the point of emergence. The degeneration rapidly 
decreased from below upwards, and at the nucleus of origin there was no 
appreciable change. 

Fifth Nerve. —There was a high degree of alteration in both sensory and 
motor portions. In the latter, the degeneration took the form of short, thin, 
black filaments with moniliform swellings mixed with swollen globules which 
could be traced into the main nucleus of origin, and for a short distance 
upwards along the mesencephalic root. 

In the former, the degeneration was of the same type but greater in degree, 
and extended in the descending root as far as the level of the seventh nucleus. 

Sixth Nerve .—There was a higher degree of degeneration in this nerve 
than in any other, and the morbid appearances were similar to those of the 
third nerve, but somewhat more advanced. The maximum of degeneration 
was found in the anterior third of the nerve between a point just posterior to 
the corpus trapezoides and the margin of the pons. In this portion the myelin 
was fused into short and long masses of somewhat sinuous outline ; some were 
completely isolated, ending in swollen bulbs, others were continued as fine 
black threads (Photo 2). Scattered at intervals there were many isolated 
finer threads and also polymorphic globules. In the middle third of the 
nerve these appearances were replaced by parallel sinuous rows of fine black 
filaments with moniliform swellings, resembling precisely the degeneration 
in the third nerve (Photo 3). Towards the nucleus of origin these filaments 
of morbid myelin became finer and fewer in number, but were easily traced 
curving round the ascending portion of the seventh nerve and ultimately 
gaining the floor of the fourth ventricle. 

Seventh Nerve .—The degeneration here was less than in the third, fifth, or 
sixth nerves, and approximated rather to that in the fourth. Its commence¬ 
ment at the point where the neurilemma sheath left the fibres was easily 
demonstrable, and it steadily decreased centralwards; in fact towards the 
nucleus there were only traces of altered myelin. The degeneration in the 
distal portion and ascending limb was mostly of the fragmentary type, with a 
few examples of filiform myelin change. 

Eighth Nerve .—The degeneration was slight and only recognisable in the 
cochlear division in the form of a few black threads with moniliform swell¬ 
ings ending abruptly lateral to the restiform body. 

Ninthy Tenthy and Eleventh Nerves .—The degeneration in these was so in¬ 
significant as to be negligible; while in the twelfth only a few blackened 
myelin threads were visible amongst the nerve strands. 

Rabbit 2.—Capsule under Skin of Cheek.—Third Nerve .—The degeneration 
was very slight. Along the course of the nerve there were flakes of altered 
myelin and short rows of globules ; fine black threads were rare. 

Fourth Nerve. —Exactly as in the third. 

Fifth Nerve: (A) Motor Portion .—Here the degeneration was of the same 

Photo 1.—Expt. 1. 3rd cranial nerve. Fine beaded myelin threads. 

1. Distal portion 

2. More central 

Photo 2.—Expt. 1. Anterior third of 6th cranial nerve, 
showing swollen globules of degenerated myelin, 
portion showing black myelin threads. 

Plate 3. 

Photo 3.—Expt. 1. Middle third of 6th cranial nerve. 1. Sinuous 
rows of fine black filaments with moniliform swellings. 

Photo 4. —Case 1. General Paralysis. 5th cranial nerve. 1. Extra¬ 
medullary portion normal. 2 . Degeneration commencing at the 
point where neurilemma is lost (intra medullary). 

Plate 14. 

Photo 5.—Expt. 2. 1. Ascending root of 5th cranial nerve, containing 

many degenerated fibres cut in transverse section. 2. 8th nerve. 
3. 7th nerve. 4. 5th nucleus. 

Photo 6.—Case 1. General Paralysis. 1. Descending root of 5th cranial 
nerve, containing many degenerated fibres cut in transvorse soc- 
tion. 2. 8th norve. 3. 7th nerve. 4. 5th nucleus. 


type as in the third nerve, but a little more marked. It commenced as soon as 
the fibres lost the neurilemma and could be traced into the main nucleus of 
origin, and for a short distance up the mesencephalic root. ( B) Sensory Portion. 
—The degeneration in this root was very intense, especially at and immediately 
inside the point where the fibres lost the neurilemma sheath. The altered 
myelin globules, some small, some laige, lay end to end in rows. Frequently 
one met as many as ten 6mall globules so arranged, and occasionally also fine 
myelin threads with moniliform swellings in parts disintegrating into fine 
black granules. In appearance the degeneration coincided with that termed 
Wallerian, and was traced in the descending root as far as the lower part of 
the medulla (Photo 5). 

Sixth Nerve .—There was more degeneration here than in the third and 
fourth nerves, and it attained its maximum in the anterior third just inside the 
corpus trapezoides. The myelin was fused into globules of varying size and 
shades of osmic acid staining, some being dark brown, others black ; but the 
blackening was never so striking, nor the myelin fusion so complete as in the 
preceding case. Even portions of the same globule varied in shade, and the 
large majority were vacuolated. Many sinuous threads were present, black 
or brown in colour, which often formed connecting bands between adjacent 
fusiform masses of degenerated myelin, or others separated by a considerable 
interval (Photo 7). Half way towards the nucleus these threads were still 
present, but absent in the posterior third of the nerve and at the nucleus 

Seventh Nerve .—The degeneration was slightly greater than in the third, 
fourth, and motor root of the fifth nerve, and was practically confined to the 
distal intramedullary portion, where the nerve emerges. Here the myelin 
had disintegrated into small and large globules arranged in rows ; there were 
a few r examples of the thread form of degeneration. 

Eighth Nerve .—The degeneration was very slight, and in the other nerves* 
ninth, tenth, eleventh, and twelfth, there was no change worthy of note. 

It is necessary to preface the description of the experiments 
on the cord by stating that in the first, in addition to placing 
a capsule under the sciatic nerve, one was implanted under the 
muscles covering the upper dorsal region. The wound here 
became septic twenty-seven days after the operation, owing to 
rupture of the capsule, and the pus invaded the cervical region 
on the right side before the accident was discovered, when the 
animal was immediately killed. 

Rabbit 3.—In the lowest segments of the cord no degeneration was 
present. In the lumbar enlargement, however, the osmic acid method yielded 
a very definite positive reaction. The degeneration of the exogenous system 
commenced immediately the fibres lost their neurilemma sheath, involved the 
root entry zone and the whole of the posterior columns with the exception of 
a small area behind the commissure, and the posterior periphery of the cord. 
There was considerable degeneration of the collaterals, most evident in those 



running through the antero-internal angle of Rolando’s substance into the 
posterior grey horns; while those passing towards the anterior cornua 
showed much less alteration (Photo 11). From the lumbar region upwards 
through the lower dorsal cord there was a steady diminution in the number 
of degenerated fibres, those remaining being scattered around the median 
septum ; but in the upper dorsal region degeneration again appeared in the 
root entry zones, especially in that of the right side. The degeneration here, 
however, had not the systematic character of that in the lumbar enlargement. 
On reaching the cervical region there was a marked increase in the number 
of degenerated fibres, these almost completely filling the posterior columns 
and leaving free the same areas as noted in the lumbar cord. The collaterals 
leaving the root entry zones were degenerated, but not further forwards than 
the level of the commissure. 

The Marchi reaction in this case was, in the large majority of instances, 
of the usual type seen in transverse section, each degenerated fibre showing 
as a solid black globule ; but occasionally appearances indicating partial 
degeneration of the myelin were met with. For example, Photo 8 shows 
a fibre in which the black degenerated outer and periaxial portions of the 
myelin are separated by a clear ring in which the osmic acid reaction is 
negative. This middle area in many other examples stained dark grey or 
brown, the colour gradually merging into the black on either side. Occasion¬ 
ally, too, the peripheral part of the myelin alone stained. In the root entry 
zones sometimes there were solid, elongated segments of degenerated myelin 
(Photo 9). In longitudinal section the degeneration showed as long parallel 
lines of myelin droplets. 

Rabbit 4.—The description of the degeneration in the above experiment 
holds good for this one with this exception, that here the morbid changes 
were not so advanced ; so that partial degeneration was very frequently 6een 
(Photo 8). The degeneration diminished rapidly on passing from the lumbar 
to the dorsal region. 

Rabbit 5.—Of the three cords this was least affected. The distribution 
of the lesion in the lumbar enlargement was the same, but the affection of 
the collaterals was much less noticeable. There were many more examples 
of partial degeneration, sometimes only three-fourths of the myelin circum¬ 
ference being blackened, leaving the remaining fourth merely darkened. 
There were many fibres in which the myelin was degenerated only round 
the axis-cylinder, the outer myelin ring remaining normal; in others this 
also was blackened, leaving a middle clear zone. The uniform degeneration 
of the whole diameter of the fibre was not found nearly so frequently as in 
the other two cords. 

The extra-medullary part of the posterior roots and of the cranial nerves 
was examined by Marchi’s method. No degenerative changes were found. In 
the cord of one case (Experiment 3) there was some degeneration of the lateral 
columns in the vicinity of the posterior horns in addition to that already 
noted in the posterior columns ; but in the pons (Experiments 1 and 2) the de¬ 
generation kept strictly to the course of the nerves with one exception, viz. 
in Experiment 1, in which there was some degeneration of the fibres of the 
corpus trapezoides for a short distance on either side of the sixth nerve. 

Plate 15. 

Photo 8.—Expt. 3. Degeneration of inner and outer parts of fibre. 

Plate 16 . 

Photo 10.—Expt. 2. 6th cranial nerve; darkening of myelin sheath 

with vacuolation. 


In discussing the nature of the degenerations above described 
it will be advantageous to commence with a motor cranial nerve. 
Taking the sixth as an example, and comparing the lesions in 
Experiments 1 and 2, we can follow the degeneration from an 
early to an advanced stage. The initial change (Experiment 2) is 
a darkening of the myelin sheath with swelling and vacuolation 
(Photo 10), passing on to the formation of the thick fusiform 
masses and thin, elongated, moniliform structures which char¬ 
acterise the later degeneration in Experiment 1. The distal 
part of the intramedullary portion of the nerve suffers first 
(Experiment 2), followed by involvement of its whole length back 
as far as the nucleus of origin (Experiment 1). Meanwhile the 
extramedullary portion remains intact. The lesioii, therefore, is 
not Wallerian, such as was present in the fifth descending root 
(Experiment 2), for, commencing distally, it extended central- 
wards and gradually diminished in that direction as the toxin 
lost potency in its progress along the nerve. Both in appear¬ 
ance and in its mode of extension this degeneration is typical of 
that found in toxic conditions, and strongly resembles in char¬ 
acter the variety known as “ segmentary necrosis.” 1 The black 
fusiform masses and long sinuous threads point clearly to an 
acute necrotic or liquefactive change in the medullary sheath. 
As to whether the axis-cylinder was involved in the process we 
cannot say without supplementing the Marchi method by other 

In the other cranial nerves and in the cord there is abundant 
additional evidence of primary myelin degeneration of varying 
degree, well exemplified in the transverse sections of the cord. 
All stages of alteration are present, from that confined either to 
the neighbourhood of the axis-cylinder or to the periphery of 
the myelin ring (Photo 8), to a more advanced phase where the 
medullated sheath is seen as a solid black globule. Where these 
globules are present in sufficient number and can be traced in a 
centrifugal direction for some distance, one must admit involve¬ 
ment of the axis-cylinder with Wallerian degeneration, e.g. in 
the fifth descending root of Experiment 2 and of Case 1, and 
in the root entry zones and collaterals of the cord in Experiment 
3. In toxic conditions, therefore, primary myelin change is the 
forerunner of secondary degeneration whose onset must be deter- 
1 Comil et Ranvier. Man. D’Hiatol. Pathol., T. 3, pp. 688, 715. 



mined either by the intensity of the toxin or by the duration of 
its action. Low virulence will account for the slow myelin 
atrophy and disintegration so often met with in many nervous 
affections, and we need only mention in this connection general 
paralysis and tabes dorsalis, in which much myelin degeneration 
can exist with comparative integrity of the axis-cylinders. But 
there comes a time when this structure’s resistance is overcome 
in the natural course of events or by a rise in virulence of the 
exciting toxin, and secondary degeneration ensues. In general 
paralysis of the acutely delirious type we have seen acute 
Wallerian degeneration in the posterior columns of the cord and 
in the cranial nerves, which could only be produced by some 
very potent toxin ; while in other chronic cases there have been 
changes ranging from simple atrophy to more advanced phases of 
degeneration. It is this variation in toxicity which constitutes 
the difference between the slow and rapid types of the above 
mentioned progressive lesions. 


(1) In peripheral nerves, spinal roots, and cranial nerves there 
is a constant stream of lymph ascending towards the central 
nervous system whose main current lies in the inner meshes or 
lymph spaces of the fibrous perineural sheath. Toxins reach the 
spinal cord and brain by this channel; and although they spread 
to some extent in the lymph spaces of the pia-arachnoid, and so 
affect structures at a distance from their point of entry, for the 
most part they pass, in the main current of the lymph, along the 
nerve roots into the substance of the central nervous system. 
Here they apparently follow the nerve paths of the affected roots, 
and show little tendency to diffuse amongst the neighbouring 
fibres (Photos 2 and 3). (2) In their extramedullary portion 

these nerves are protected from the influence of the toxins by 
the vital action of the neurilemma sheath, but on losing this in 
their intramedullary part they at once undergo degeneration. 
(3) The first change is a primary degeneration of the myelin ; 
the axis-cylinders and nerve cells are evidently affected later. 

Since writing the above, we have met with and are now 
investigating a case of general paralysis which bears out to a 
very marked degree the experimental and clinical evidence given 


above. At the autopsy the following morbid appearances were 
found, suggesting the presence of some infective condition, e.g. 
acute catarrh and ulceration of the large intestine with haemor¬ 
rhages, especially of its lower portion, chronic thickening of the 
mucous membrane of the bladder, with an acute cystitis and very 
offensive blood-stained urine. In addition we should mention 
the presence of a septic condition of the right knee-joint which 
had existed for two weeks previous to death. Cultures were 
made from the cerebro-spinal fluid of the lateral ventricles and 
of the lumbar region, and yielded an abundant growth of a rod- 
shaped bacillus which often assumed a long thread-like form. In 
sections of the right sciatic nerve we failed to find any organisms, 
but found them abundantly in the following regions, viz.: in 
the internal layers of the perineural sheath of the posterior and 
anterior lumbar roots, amongst the fibres of the posterior root 
entry zone, in the pia-arachnoid around both sides of the cord, 
and in the septa passing into the cord where they were most 
numerous at the periphery, amongst the anterior root fibres, and 
a few in the central canal and surrounding tissues. In the spinal 
roots the organisms also followed the track of the vessels passing 
into the centre of the nerves. In both roots and cord there were 
many in the adventitial lymph spaces of the vessels, but nowhere 
did we observe a single organism within the lumen. The vessels 
were dilated, and there was cellular infiltration of their walls. 
In the cord the organisms were found to be limited to those 
areas which we have shown to be affected as a result of toxic 
absorption (8). This is especially well illustrated in comparison 
with a case of brachial neuritis (10). It will be seen here that 
the distribution of the myelin degeneration in the posterior root 
entry zone, the anterior radicular zone, around the pia-arachnoid, 
and along the septa to the central parts of the white matter, 
coincides exactly with that of the organisms in the present case. 

The presence of the organisms in the adventitial sheath of 
the vessels and their entire absence within the lumen are facts 
of very great significance. We would suggest that this infection 
of the adventitia is secondary to the infection of the lymph 
circulating amongst the nerve fibres. In support of this view 
we would mention that it is frequently found, in advanced phases 
of cord degeneration, that the fatty products in process of 
granular disintegration and absorption pass into the adventitia 



and fill the cells and spaces there until the vessel wall may be 
stained almost uniformly black with osmic acid. It is possible 
that this is the true explanation of the vascular changes found 
in the cord in acute myelitic lesions, and that these should not 
be considered as being of primary hsematogenous origin, but as 
being reactive changes due to a primary lymphogenous infection 
of the adventitia of the vessel walls. 


1. Orr and Rows. Brain , Winter, 1904. 

2. Levi. Arbeit, a. d. neur. Instit. a. d. Wien. UniversittU , Bd. 13, 1906. 

3. Marie et Morax. Quoted in Cornil et Ranvier, Man. D’Hist. Pathol., 
T. 3, p. 721, 1907. 

4. Homen and Laitinen. See Hom^n, Arbeit, a. d. path. Instit. zu Helsing 
fore (Finland), 1902. 

6. Pirrone. Rif. Med., 1905. 

6. Guillain. Comil et Ranvier, T. 3, p. 719. 

7. Sicard and Bauer. Comil and Ranvier, T. 3, p. 719. 

8. Orr and Rows. Rev. Neurol, and Psych., Jan. 1906. 

9. Medea. Riv. Speriment. di Fren. Fasc., 1 and 2, 3 and 4, 1906. 

10. Orr. Rev. Neurol, and Psych., October 1903. 




In the account of the crus cerebri in Testut’s “ Traits d’Anatomie 
humaine” (tome ii., 1900, p. 598), it is stated that the bundles 
of fibres of which the cerebral peduncles are composed are 
usually arranged in a parallel manner, but “ dans certains cas les 
faisceaux nerveux obliquent en masse d’arri&re eu avant et de 
dedans en dehors, com me si le p4doncule 4tait tordu sur son axe ”; 
and, further, “ dans d’autres cas, on voit les fibres les plus in¬ 
ternes abandonner brusquement leur situation primitive, croiser k 
la manure d’une ^charpe la face infdrieure du pddoncule pour 
venir occuper son cot4 externe (fig. 469, 3): ce faisceau oblique, 
auquel F£r]S a donn4 le nom de faisceau en tcharpe, est rarement 



symdtrique.” Testut’s account then goes on to distinguish this 
“ sling-band ” from the taenia pontis of Henle and the tractus 
peduncularis transversus of v. Gudden. 

In the accompanying drawing of the left lateral aspect of the 
mesencephalon of a Soudanese negress (Fig. 1), all three bands 
are present. The “ Faisceau en 
&charpe ” is labelled “ Fasc. obi. 
cruris ” a contraction of the 
descriptive term “ Fasciculus 
obliquus cruris cerebri with 
which I propose to distinguish 
the bundle in question. It 
obviously consists of some of 
the most lateral fibres of the crus 
cerebri which dissociate them¬ 
selves from the rest of that Tr.^t- }'f$ 

body, and, after passing ob¬ 
liquely downward (caudally) and 
inward on the surface of the 
crus, enter the interpeduncular 

„„„„„ „ i i_ _.• „n„ Fig. 1 —The left lateral aspect of the 

Space and plunge vertically mesencephalon of a Soudanese negress. 

downward into the substance of 
the pons varolii. The rest of 
its course is shown in the accompanying photograph of a 
sagittal section of the same brain (Fig. 2) as a very distinct, 
bow-shaped, white strand along the line of separation of the 
pontine fibres from the formatio reticularis. In this section 
the pontine region was cut about one millimetre to the left 
of the mesial plane, and thus revealed this fasciculus (which is 
present only on the left side) with extraordinary clearness. 
Without any further preparation, a vast number of tree-like 
bundles of fibres were clearly visible passing forward into the 
pons (Fig. 3), to terminate presumably in the nuclei pontis. No 
fibres could be detected passing backward into the formatio 

For the purpose of locating this bundle more accurately, the 
two halves of the mesially-split pons were put together and cut 
in transverse section. The fasciculus obliquus cruris was thus 
exposed lying in the formatio reticularis in close apposition to 
the inner extremity of the mesial fillet (Fig. 4, lemniscus), 

\ Fast. ok 


Tt. pdvnc. traits. 

36jpoalon of a Soudanese negress. 
Fasc. obi. cruris is the “Faisceau en 
kharpe ” of F6 r& 



with which it might easily be confused in studying transverse 

The fasciculus obliquus cruris is clearly a part of the 
peduncular system ending in the nuclei pontis. In this 
particular specimen I was unable to trace the bundle higher 
than the corpus geniculatum laterale, under which it emerged 

Fig. 3. Fio 4. 

Fig. 3.—A semi-diagrammatio representation of the fibres exposed in the left half 
of the pons that was removed from the specimen shown in Fig. 2. 

Fig. 4.—Part of a transverse section through the pons shown in the other three 
figures. The section passes through the insertion of the trigeminal nerve (Ntrv. F.), 
and exposes the fasciculus obliquus cruris on the left side of the mesial raphd, near the 
inner ^and of the lemniscus. The posterior longitudinal bundle is shown but not 

from the cerebrum (Fig. 1); but in other brains that I specially 
examined for this purpose I could trace the fibres of the extreme 
lateral part of the crus into the temporal region of the hemi¬ 
sphere. It is most probable that the fasciculus obliquus is part 
of the path connecting the temporal region of the left cerebral 
hemisphere with the right cerebellar hemisphere. 

Taking three other human brains at random, I found this 
u oblique bundle in two of them j and in all three cases it occurred 
on the left side. In one specimen only there was a small bundle 
on the right side. In none of the specimens examined have I 
been able to demonstrate its mode of termination with the 
clearness exhibited in the chance-section shown in Figs. 
2 and 3. 

The apparent predilection of this bundle for the left side is 
interesting, especially when it is recalled that the aberrant 
circumolivary bundle of the pyramidal tract is found only on the 

Platk 18. 

Fig. 2. —Untouched photograph of a sagittal section of the same brain, showing the terminal portion of the fasciculus 
obliquus cruris. This section passes through the pontine region, one millimetre to the left of the mesial plane. 



left side in the vast majority of cases (see Review of Neurology 
and Psychiatry, vol. ii., No. 5, May 1904, p. 377). Among 
more than one hundred examples of the latter anomaly I have 
seen only three cases in which it was present only on the right 
side. It seems as if there were a distinct tendency for fibres 
to be crowded out of the left peduncular tract into aberrant 




During the week that has elapsed since I posted the account of 
the aberrant course of a part of the left cerebro-pontine tract 
for publication in this Journal, I have examined twenty-five 
brains, and found ten examples of a similar anomalous bundle. 
In every case it occurred on the left side: in one case a smaller 
bundle of the same nature was found on the right side, and in 
another case symmetrical aberrant bundles were found. 

During the course of the search for the “faisceau en dcharpe," 
I have found a most curious anomaly of a serially homologous 
bundle of fibres, which is represented in the accompanying 
diagram and photographs. 

It was found on the left side only. At the junction of the 
lower and middle thirds of the pons a large vertical band of 
fibres was seen emerging (Fig. 1, x ) between the transverse 
pontine fibres just to the left of the groove for the basilar artery, 
and passing downward on the surface of the pons. At the 
lower border of the latter the fibres became collected into a 
prominent round cord, which plunged horizontally into the 
substance of the hind-brain. A vertical section through this 
curious anomaly, about 3 mm. from the mesial plane (Fig. 2), 
clearly reveals its nature: it is the most superficial of the 
bundles prolonged downward through the pons from the pedun- 
culus cerebri. In a second vertical sagittal section, about 1 mm. 
from the mesial plane (Fig. 3), the further course of the bundle 
can be seen horizontally backward below the pontine fibres, and 
then upward between the latter and the formatio reticularis, to 
end, like the “ faisceau en icharpef which is also present in 
this specimen (Fig. 2), in the nuclei pontis. 





It is generally accepted that the deltoid muscle, flexors of the 
elbow and supinator longus are innervated chiefly from the fifth 
cervical segment of the cord, and that the intrinsic muscles of 
the hand receive their nerve supply from the first dorsal and 
eighth cervical segments. According to most clinical records, 
the pronators are represented at about the same level of the 
cord as the triceps, which is generally placed at the sixth or 
sixth and seventh cervical segments; the extensors of the wrist 
and long extensors of the fingers are usually grouped together at 
the level of the seventh cervical segment, somewhat lower than 
the triceps but higher than the flexors of the wrist and long 
flexors of the fingers, which are also usually grouped together 
and placed at the eighth cervical segment. 

I have recently had a case of fracture of the cervical spine 
which appears worthy of record as showing, with almost experi¬ 
mental precision, the relative order of innervation of certain arm 
muscles. Operation and, later, autopsy, disclosed fracture of the 
body of the sixth cervical vertebra, with a comminuted fracture 
of the left lamina of the fifth and the right lamina of the sixth 
vertebra. There was no complete division of the cord, but 
microscopical examination showed an almost complete crush at 
the seventh cervical segment, while the eighth segment had also 
been greatly compressed. Even macroscopically it was evident 
that the upper limit of the cord lesion was higher on the left 
side—there was no obvious implication of the sixth segment on 
the right side, while the lower part of this segment was clearly 
involved on the left side. This difference on the two sides was 
confirmed by microscopical examination: on the right side the 
grey matter of the sixth segment appeared intact, while on the 
left side the lower part of the sixth segment had shared in the 
crush, and even the upper part was greatly distorted and the 
ganglion cells of the anterior horn were markedly diminished in 
number and abnormal in appearance. The fifth segment was 
intact on both sides; no lesion other than the crush, e.g. an 
isolated focus of haemorrhage, could be found. 


Clinically, there was complete and permanent loss of motion 
and sensation on all parts innervated below the site of lesion: 
the breathing was entirely diaphragmatic. In view of the site 
and severity of the lesion, the duration of life appears 
remarkable : the patient lived 355 days. 

The condition of the arms, as regards motor power, was as 

Muscles of shoulder 
Flexors of elbow V 

Supinator longus J 

Extensors of wrist 



Extensors of fingers ' 
Flexors of wrist 
Flexors of fingers 
Intrinsic muscles of 


Good power throughout. 

Very fair power from the 
first, which improved. 
No certain power at first, 
later, fair power. 

No power at first, ?? 
slight power later. 

No power throughout. 


Good power throughout. 

Practically no power at 
first, slight power later. 
No power. 

No power. 

No power throughout. 

In view of this distribution of the motor paralysis in the 
arms and of the situation of the lesion in the cord, this case 
appears to warrant the following conclusions:— 

(1) The extensors of the wrist are represented in the cord at 
a level higher than the triceps, the former almost certainly at 
the sixth cervical segment, the latter below this segment. 

(2) The pronators are represented below the extensors of 
the wrist and above the triceps, probably at the sixth and 
seventh cervical segments. 

(3) The extensors of the wrist are represented at a higher 
level than the extensors of the fingers. 

(4) The extensors of the wrist are represented at a higher 
level than the flexors of the wrist. 

Stewart and Turner {Brain, 1900, p. 139) record a case 
of dislocation of the fifth cervical vertebra forward on the sixth, 
with severe crush of the cord at the upper level of the seventh 
cervical segment; the distribution of motor paralysis in the arms 
was very similar to that noted in my case, with this exception, 
that the flexors as well as the extensors of the wrist remained 
intact. Stewart concludes that these two groups of muscles are 



grouped together at a level of the cord higher than the seventh 
cervical; my case does not confirm this conclusion. 

It may be of interest to place in tabular form the conclusions 
as to the segmental or root supply of the arm muscles arrived at 
by such writers as Ferrier and Yeo (1) (experimental), Herring- 
ham (2) (anatomical), Gowers (3), Thorburn (4), Kocher (5), 
Starr-Edinger (6), Oppenheim (7), Horsley (8), Purves Stewart 
(loc. tit.). 

Ferrier and Yeo. 











Triceps . . 

Extensors of 



chiefly 7 







chiefly 7 

wrist . . 

Long exton- 
so r s of 




chiefly 6 




6, 7 

chiefly 7 



fingers . . 



6, 7 




6, 7 

chiefly 7 



Flexors of 










wrist . . 

Long flexors 

6,8 j 




i 7 





of fingers . 

7,8 j 


_ ' 






The numbers refer to cervical segments or roots. 

Analysing these results from the point of view of the four 
conclusions drawn from my case, we find that— 

(1) Ferrier and Yeo on experimental grounds, and Herring- 
ham from anatomical data, place the extensors of the wrist 
higher than the triceps; Gowers and Stewart arrive at the same 
conclusion, but most clinical records place the triceps either 
higher than the extensors of the wrist (Thorburn, Kocher) or at 
the same level (Starr-Edinger, Oppenheim, Horsley). 

(2) The writers quoted are generally agreed in placing the 
pronators at or about the same level as the triceps. 


(3) Most of the writers who specially note the point (Ferrier 
and Yeo, Gowers, Starr-Edinger, Oppenheim, Horsley) place the 
extensors of the wrist and long extensors of the fingers together 
at a common level; Kocher and Stewart place the former at a 
higher level than the latter, and Campbell Thomson (Brain, 
1899, p. 136) records a case which strongly supports this view. 

(4) Most of the authors quoted (Ferrier and Yeo, Gowers, 
Thorbum, Starr-Edinger, Oppenheim, Horsley) place the flexors 
of the wrist below the extensors of the wrist; Kocher and 
Stewart place them at the same level. 


1. Ferrier and Yeo. Proc. Roy. Soc 1881, 1883. 

2. Herringham. Proc. Roy. Soc., 1886. 

3. Gowers. “ Diseases of the Nervous System,” vol. L, ed. 3, p. 252. 

4. Thorbum. “A Contribution to the Surgery of the Spinal Cord,” 
1889, p. 4. 

5. Kocher. MittheiL aut den Gremgebieten der Med. und Cheir., 1897. 

6. Starr-Edinger. “ Edinger’s Anatomy of the Central Nervous System,” 
1899, p. 336. 

7. Oppenheim. “Lehrbuch der Nervenkrankh.,” 1898, p. 113. 

8. Horsley. “ Allbutt’s System of Medicine,” voL vL, p. 859. 



(192) ROLANDO. David Waterston, Joum. of Amt. and Phys., 
Vol. xli., p. 143. 

In this communication is recorded an account of the brain of a 
newly-born child in which the fissure of Rolando in each hemi¬ 
sphere was interrupted near its centre by a short gyrus connecting 
the precentral with the postcentral gyrus. 

This condition has been met with in some instances in the 
adult brain, but has not hitherto been proved to be present at 
birth. Author’s Abstract. 




THE CALL OF SOCRATES. (La Vocation do Socrate. Specimen 
(193) d’nne application de la science psychologize k celle de 

l’histoire.) Pierre Bovet, Arch, de Psychol., Jan. 1907, 

p. 261. 

This paper is a clever and plausible attempt to whitewash the 
Delphic Oracle, and incidentally a reminder of the reservation, 
somewhat of a disappearing mirage in these days of the pre¬ 
dominance of the devotedly documentary school of historians, 
that the splendidly scrupulous methods of the jficole des Chartes 
may profit betimes by the application of the accessory sciences 
of mind to that synthetic interpretation of the scoriae of tradition 
which even more than the aggregation of guaranteed facts is (as 
Polybius pointed out long ago) the highest function of the historian. 
Paradoxically the thesis it chances to sustain involves the 
straightening out by one rationalist organon of the twist inflicted 
by another, and the restoration of credit to an admittedly authentic 
text which the commentators have felt obliged to explain away. 

Agreed as to the historical truth of Plato’s chapter recounting 
the solicitation of the opinion of the Oracle by Cheirephon, both 
Zeller and Gomperz are also at one in holding that the deliverance 
merely confirmed in Socrates an already formed conviction of 
a special mission, and had no direct influence on the awakening 
of his dialectic genius. Both critics go in the teeth of the text 
to make the absolute assumption that Socrates was already a 
well-known personage whose reputation was made. M. Bovet 
denies the judiciousness of this attitude. Reconstituting the scene 
on the lines of Monceaux’s article in Daremberg and Saglio’s 
Dictionnaire des Antiquitis, he suggests that whereas Zeller, and 
especially Gomperz, envisage exclusively the priests of the shrine, 
cold, calculating, prudent office-holders, concentration of the 
attention on the Pythia herself transforms the problem into 
one in the psychology of ecstatics. The transaction is then 
resolved into a simple case of what in po